Search

Elevated sympathetic activity and chronic inflammation are known contributory factors observed in hypertension. We have observed that sympathoinhibitory electroacupuncture (SI-EA) at acupoints ST36-37 alleviates sympathetic activity and hypertension. Additionally, EA at acupoints SP6-7 exerts anti-inflammatory (AI-EA) effects. However, it is not known whether simultaneous stimulation of this combination of acupoints attenuates or enhances individual effects. A 2 × 2 factorial design was used to test the hypothesis that combining SI-EA and AI-EA (cEA) leads to greater reduction of hypertension by decreasing sympathetic activity and inflammation in hypertensive rats than either set of acupoints alone. Dahl salt-sensitive hypertensive (DSSH) rats were treated with four EA regimens including cEA, SI-EA, AI-EA, and sham-EA twice weekly for five weeks. A group of normotensive (NTN) rats served as control. Systolic and diastolic BP (SBP and DBP) and heart rate (HR) were measured non-invasively by tail-cuff. Plasma norepinephrine (NE), high-sensitivity C-reactive protein (hs-CRP) and interleukin 6 (IL-6) concentrations were determined with ELISA at the completion of treatments. DSSH rats on high salt diet progressively developed moderate hypertension within five weeks. DSSH rats treated with sham-EA showed continuous increase in SBP and DBP and elevations in plasma NE, hs-CRP, and IL-6 levels relative to NTN control. Both SI-EA and cEA decreased SBP and DBP, and had corresponding changes in biomarkers (NE, hs-CRP, and IL-6) compared with sham-EA. AI-EA prevented SBP and DBP elevation and decreased IL-6 and hs-CRP relative to sham-EA. Importantly in DSSH rats that received repetitive cEA treatment, SI-EA interacted positively with AI-EA leading to greater reduction of SBP, DBP, NE, hs-CRP, and IL-6 than SI-EA or AI-EA alone. These data suggest that by targeting both elevated sympathetic activity and chronic inflammation, cEA regimen results in a greater reduction of BP effects in treating hypertension compared to using individual SI-EA or AI-EA alone.

Significance: Inflammation is a normal response to injury, but uncontrolled inflammation can lead to several diseases. In recent years, research has shown endogenously synthesized hydrogen sulfide (H2S) to be a novel mediator of inflammation. This review summarizes the current understanding and recent advances of H2S role with respect to inflammation in different diseases. Recent Advances: Promising early results from clinical studies suggest an important role of H2S in human inflammatory disease. Critical Issues: Defining the precise mechanism by which H2S contributes to inflammation is a complex challenge, and there is active ongoing research that is focused on addressing this question. Most of this work has been conducted on animal models of human disease and isolated/cultured cells, and its translation to the clinic is another challenge in the area of H2S research. Future Directions: Defining the mechanism by which H2S acts as an inflammatory mediator will help us better understand different inflammatory diseases and help develop novel therapeutic approaches for these diseases.

Medicinal plants play significant roles in the prevention of human beings from various pathogenic microorganisms and diseases. The immunomodulators are agents used to modulate the immune system and can be obtained from both natural as well as synthetic origin from plants and chemicals. Alteration within the system is often achieved by immunomodulatory agents from a plant source, low molecular weight compounds like alkaloids and other nitrogen-containing compounds, terpenes, phenols, and high molecular weight compounds like lectins, polysaccharides. The Immune system is a part of the body to detect the pathogen by using a specific receptor to produce an immediate response by the activation of immune components cells, cytokines, and chemokines and also release of an inflammatory mediator. This review also discusses various ethnopharmacological information of traditional medicinal plants being used as immunomodulators.

Bahan alam merupakan sumber senyawa aktif dan obat yang baik. Kajian kandungan tumbuhan sangat menarik dalam ditemukannya senyawa aktif terutama untuk terapi pada penyakit asma. Asma merupakan penyakit kronis dengan gejala mengi, sesak napas, dada sesak, dan batuk. Ada beberapa mekanisme kerja senyawa anti-asma, yaitu penghambat reseptor H1 dan H2, penurunan kadar imunoglobin E, mediator inflamasi, pencegahan sekresi sitokin Th2, dan mekanisme spesifik lainnya. Metode yang digunakan berupa tinjauan pustaka. Studi tinjauan pustaka dilakukan dengan mencari beberapa kata kunci seperti tumbuhan herbal, anti-asma, medicinal plants, antiasthmatic activity, dan lain-lain pada database elektronik termasuk ClinicalKey, Science Direct, PubMed, dan Google Scholar. Data yang diperoleh dikumpulkan, dianalisis, dan disimpulkan sehingga didapatkan data dan penjelasan tentang tumbuhan potensial yang ditemukan di seluruh Asia sebagai sumber alternatif pengobatan asma. Tiga puluh jenis tumbuhan obat tradisional di Asia yang berpotensi memiliki aktivitas anti-asma berhasil diperoleh dengan berbagai macam mekanisme kerja. Data mengenai aktivitas tumbuhan yang dikumpulkan dalam tinjauan pustaka ini menunjukkan penggunaannya sebagai bagian dari strategi pengobatan herbal alternatif dan sumber pengobatan asma.

The effect of resveratrol, a free radical scavenger, during cataract development was evaluated in the Wistar rat pup model. This study investigated the possible free radical scavenging potential of resveratrol at 40 mg/ kg body wt dose in selenite-induced cataract in rat pups. Intraperitoneal injection of sodium selenite (15 µm mol/ kg body wt) in 8 to 10 day old rat pups lead to severe oxidative stress in the tissues evidenced by decreased antioxidants and increased lipid peroxidase, nitric oxide, superoxide anion, hydroxyl radical generation, inducible nitric oxide synthase (iNOS) as well as nuclear factor kappa B (NF-kB) expression levels that probably led to cataract formation. Selenite exposure also caused an increase in total calcium in the eye lens and significantly inhibited the activity of Ca2+ ATPase but not Na+/ K+ ATPase or Mg2+ ATPase. However, both pre- and co-treatments with resveratrol, but not post-treatment, led to an increase in antioxidant levels with a concomitant reduction in oxidative stress and also rescued the selenite-mediated increase in lens Ca2+ and inhibition of Ca2+ ATPase activity in the eye lens. The results of this study demonstrate antioxidants decrease and increase in free radical generation triggered by selenite causes the inactivation of lens Ca2+ ATPase leading to a rise in intracellular Ca2+ level. Resveratol treatment was able to prevent selenite-induced oxidative stress and in turn the inhibition of lens opacification. Thus, resveratrol has the potential to function as an anti-cataractogenic agent, possibly by preventing free radical-mediated accumulation of Ca2+ in the eye lens.

Myocardial ischemia reperfusion syndrome is a complex entity where many inflammatory mediators play different roles, both to enhance myocardial infarction-derived damage and to heal injury. In such a setting, the establishment of an effective therapy to treat this condition has been elusive, perhaps because the experimental treatments have been conceived to block just one of the many pathogenic pathways of the disease, or because they thwart the tissue-repairing phase of the syndrome. Either way, we think that a discussion about the pathophysiology of the disease and the mechanisms of action of some drugs may shed some clarity on the topic.

This study describes anti-inflamatory activity of epicuticular wax (ECW) extracted from leaves of Eugenia brasiliensis Lam., and its isolated compounds, catechin and gallocatechin in a pleurisy model in mice. The results for exudation and cell migration showed that the extract and isolated compounds from the plant were effective in inhibiting these inflammatory parameters. The ECW demonstrated a dose-dependent effect on the inhibition of cell migration. The results for NOx levels reveals that the isolated compounds from Eugenia brasiliensis were effective in inhibiting the production of this inflammatory mediator, however, ECW were not able in inhibiting the production of NO in the pleural cavity, at the tested doses. The results here obtained, helps to reinforce the scientifically hypothesis that E. brasiliensis has an important anti-inflammatory activity, and that this effect may be, at least in part, by the presence of the compounds catechin and gallocatechin.

Inflamm-aging - the term, describes the development of chronic inflammation during aging without the infection pathology. It is supposed, that inflamm-aging is one of the reason of age-related pathology, partially, Alzheimer disease (AD). There were done comparative analysis of AD (Аβ42, τ-protein, р16) and inflammation (IL-6, TGFα, NF-kB) markers in hippocamp and blood lymphocytes in elderly and old people. It was shown, that expression of investigated signal molecules in hippocamp and lymphocytes of elderly and old AD people increased in comparison with people of control group (without neurodegenerative pathology). Thus, inflammation mediators play important role in AD pathogenesis and can be the potential target for neuropathology therapy.

Zinc oxide (ZnO) is the most efficient curing activator employed in the industrial rubber production. However, ZnO and Zn(II) ions are largely recognized as an environmental hazard being toxic to aquatic organisms, especially considering Zn(II) release during tire lifecycle. In this context, aiming at reducing the amount of microcrystalline ZnO, a novel activator was recently synthetized, constituted by ZnO nanoparticles (NPs) anchored to silica NPs (ZnO-NP@SiO2-NP). The objective of this work is to define the possible hazards deriving from the use of ZnO-NP@SiO2-NP compared to ZnO and SiO2 NPs traditionally used in the tire industry. The safety of the novel activators was assessed by in vitro testing, using human lung epithelial (A549) and immune (THP-1) cells, and by the in vivo model zebrafish (Danio rerio). The novel manufactured nanomaterial was characterized morphologically and structurally, and its effects evaluated in vitro by the measurement of the cell viability and the release of inflammatory mediators, while in vivo by the Fish Embryo Acute Toxicity (FET) test. Resulting data demonstrated that ZnO-NP@SiO2-NP, despite presenting some subtoxic events, exhibits the lack of acute effects both in vitro and in vivo, supporting the safe-by-design development of this novel material for the rubber industry.

Systemic mastocytosis with associated primitive myelofibrosis is a rare and complex disease with a difficult therapeutic management. The release of several inflammation mediators can trigger acute cardiovascular events.

Background and aim of the study The aim of this study is to evaluate the changes in the inflammatory mediator's serum amyloid A (SAA), adiponectin, and resistin in the serum of patients with stable angina and acute myocardial infarction. Subjects and methods The study was done on 60 subjects divided into three groups: 20 healthy normal individuals as a control group, 20 patients with stable angina (atherosclerotic plaque), and 20 patients with myocardial infarction. Fasting blood samples were withdrawn from all subjects and serum was prepared. SAA, resistin, and adiponectin levels were quantitatively measured by enzyme-linked immunosorbent assay (ELISA). Results The SAA level was significantly higher in both stable angina and the acute myocardial infarction group than the control group (2.7179 ± 0.44501 mg/L) and the serum resistin level was significantly higher (p-value = 0.0) in the stable angina (8.368 ± 1.633 ng/ml) and the acute myocardial infarction (13.606 ± 2.067 ng/ml) groups (p-value= 0.0) than the control group. (2.4272±1.25210 ng/ml). Moreover, resistin levels in stable angina when compared to the AMI showed a significant difference between them (p-value = 0.0) while adiponectin was significantly lower in the acute myocardial infarction group. (6.641±2.6011 µg/mL, p-value = 0.019) than its level in the control group (11.873±1.798 µg/mL). While the adiponectin level showed no significant differences between stable angina in comparison to the AMI. Conclusion SAA can be used as a confirmatory marker for stable angina and a diagnostic tool for AMI patients. Both SAA and resistin may participate in the atherosclerosis process as an effectors molecule of inflammatory reactions. For adiponectin, we concluded that it has the antiatherogenic property and its levels were lower in both the stable angina and acute myocardial infarction groups.

Background Challenges of diagnosing and treating sepsis only seem more difficult as incidence increases, patients become older and sicker, and pathogenic organisms evolve. New understanding of inflammatory mediators and pathways, immunity, and genetic variability in this disease state suggests that the current definitions of SIRS, sepsis, severe sepsis, and septic shock are oversimplified. Objective The aim of our study is to evaluate the level of RDW, CRP and clinical scores "SOFA and APACHI" as markers in patients with sepsis and their levels on the outcome and resolution of sepsis in ICU. Methodology We conducted a prospective observational controlled study on 90 adult persons of both sex, 45 of them are adult patients and served as the study group (Group I), and the other 45 are healthy adult volunteers and served as the control group (Group II). The study group represented patients admitted to the ICU of Intensive Care Unit at Damanhour Medical National Institute who fulfilled the diagnostic criteria for sepsis, severe sepsis and septic shock on arrival to ICU according to the SCCM/ ESICM/ ACCP/ ATS/SIS International Sepsis Definitions Conference. Results. In the present study we found that CRP measured on admission was not a predictor of mortality, while that measured at day 5 and day 10 predicted mortality, where there was no statistically significant difference in CRP levels between survivors and non-survivors at the day of admission while there were statistically significant differences between survivors and non survivors according to CRP levels at day 5 (p = 0.001*) and at day 10 (p = 0.001*). It was found also that there were statistically significant differences between survivors and non-survivors according to RDW at day 1(p = 0.011*) and at day 5(p = 0.009*), at day 10 was found there was no statistically significant difference between survivors and non-survivors (p = 0.338). Conclusion RDW is a new promising cheap and readily available biomarker that can be able to diagnose patients with sepsis with accuracy comparable to CRP. Also, RDW at admission is able to predict mortality.

A Selenium (Se) is an element belonging to the nonmetallic group. It was first discovered in 1817 by J.J. Berzelius. Until the 1950s, it was considered to be toxic to animals. However, with increasing research conducted on laboratory animals, it is now clear that Se is necessary for the proper functioning of both plants and animals. Recent studies indicate that Se is necessary for the proper functioning of metabolic pathways in animals. It was evidenced that Se is a component of about 100 proteins involved in the immune system, antioxidant homeostasis, or release of an inflammatory mediator. Therefore, it is of key interest to find the appropriate dosage for the supplementation of Se in the diet of farm animals and thereby eliminate physiological disorders in the body associated with Se imbalance. In this study, we present a literature review on the importance and appropriate dosage of Se in the diet of poultry concerning their health status, production results, and the quality of animal-origin products.

Allergic mechanisms account for most cases of chronic rhinitis. This condition is associated with significant impairment of quality of life and high indirect costs. The identification of the allergic triggers of rhinitis has been historically based on the performance of atopy test [skin prick test (SPT) and serum allergen-specific (s)IgE]. Nevertheless, these tests only denote sensitization, and atopy and allergy represent two different phenomena. It is now clear that allergic phenotypes of rhinitis can exist in both atopic (allergic rhinitis, AR) and non-atopic (local allergic rhinitis, LAR) individuals. Moreover, both allergic phenotypes can coexist in the same rhinitis patient (dual allergic rhinitis, DAR). Therefore, a diagnostic approach merely based on atopy tests is associated with a significant rate of misdiagnosis. The confirmation of the allergic etiology of rhinitis requires the performance of in vivo test like the nasal allergen challenge (NAC). NAC is mandatory for the diagnosis of LAR and DAR, and helps decide the best management approach in difficult cases of AR. Nevertheless, NAC is a laborious technique requiring human and technical resources. The basophil activation test (BAT) is a patient-friendly technique that has shown promising results for LAR and DAR diagnosis. In this review, the diagnostic usefulness for chronic rhinitis of SPT, NAC, olfactory tests, serum sIgE, BAT and the quantification of inflammatory mediators in nasal samples will be discussed. The accurate performance of an etiologic diagnosis of rhinitis patients will favor the prescription of specific therapies with disease-modifying potential like allergen immunotherapy.

A significant proportion of COVID-19 patients are suffering from prolonged Post-COVID-19 Fatigue Syndrome, with characteristics typically found in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). However, no clear pathophysiological explanation, as yet, has been provided. A novel paradigm for a Post-COVID-19 Fatigue Syndrome is developed here from a recent unifying model for ME/CFS. Central to its rationale, SARS-CoV-2, in common with the triggers (viral and non-viral) of ME/CFS, is proposed to be a physiologically severe stressor, which could be targeting a stress-integrator, within the brain: the hypothalamic paraventricular nucleus (PVN). It is proposed that inflammatory mediators, released at the site of COVID-19 infection, would be transmitted as stress-signals, via humoral and neural pathways, which overwhelm this stress-center. In genetically susceptible people, an intrinsic stress-threshold is suggested to be exceeded causing ongoing dysfunction to the hypothalamic PVN's complex neurological circuitry. In this compromised state, the hypothalamic PVN might then be hyper-sensitive to a wide range of life's ongoing physiological stressors. This could result in the reported post-exertional malaise episodes and more severe relapses, in common with ME/CFS, that perpetuate an ongoing disease state. When a certain stress-tolerance-level is exceeded, the hypothalamic PVN can become an epicenter for microglia-induced activation and neuroinflammation, affecting the hypothalamus and its proximal limbic system, which would account for the range of reported ME/CFS-like symptoms. A model for Post-COVID-19 Fatigue Syndrome is provided to stimulate discussion and critical evaluation. Brain-scanning studies, incorporating increasingly sophisticated imaging technology should enable chronic neuroinflammation to be detected, even at a low level, in the finite detail required, thus helping to test this model, while advancing our understanding of Post-COVID-19 Fatigue Syndrome pathophysiology.

Aims: Gestational diabetes (GDM) is carbohydrate intolerance occurring in pregnant women. In the GDM pathogenesis, the low-grade inflammation plays a significant role. Various inflammatory mediator...

This work aimed to obtain and characterize protease inhibitors from A. colubrina leaves and evaluate their potential as inflammatory mediator and cell viability. The protein extract was analyzed and characterized by SDS-PAGE, RP-HPLC-PDA, MALDI-TOF/MS and Zeta potential. Bioassays were conducted in order to evaluate the cell viability in RAW 264.7, in vitro (NO and TNF-α production inhibition) and in vivo anti-inflammatory potential, inhibition rate of trypsin and hemagglutination activity from protein extract. The results revealed the presence of bands at 14, 21 and 30 kDa in SDS-PAGE, the RP-HPLC-PDA analysis showed peaks at 12, 13, 28 and 40 minutes and MALDI-TOF/MS showed peaks with 3.4, 4.7, 5.6, 9.4 and 11.2 kDa. The protein extracts presented enzymatic activity inhibition of trypsin (IC50 59.2 μgmL−1), did not show any cytotoxicity to RAW264.7 cells, hemagglutination 8HU and insignificant reduction in NO and TNF-α production and reduced anti-inflammatory potential in vivo compared to dexamethasone.

BACKGROUND: Chronic rhinosinusitis with nasal polyps (CRSwNP) remains a challenging clinical entity with its propensity for recurrence. This disease decreases the patients’ quality of life and creates a high economic burden. An effort to investigate the aetiology of recurrent polyps have to be more alert. AIM: This study aims to prove the differences in expression of IL-5, IL-8, IL-17A and TGF-β1 in mucosal and polyp tissue between CRSwNP and recurrent CRSwNP and also to determine which expression of cytokines that have the main role in mucosal and polyp tissue in recurrent CRSwNP. MATERIAL AND METHODS: An observational study was conducted with a comparative cross-sectional design of CRS patients with 15 recurrent CRSwNP and CRSwNP who had never undergone surgery for as many as 15 polyps. Mucosal specimens of nasal polyps are taken by brushing, and polyp tissue specimens are taken during surgical removal of nasal polyps. Specimens from the polyp mucosa were examined by ELISA while the polyp tissue specimens were carried out immunohistochemistry (IHC). RESULTS: The result showed that there is a significant difference in IL-5 expression in the polyp mucosal between CRSwNP with recurrent CRSwNP, where expression is higher in recurrent CRSwNP. The expression of IL-8, IL-17 and TGF-β1 were lower in recurrent CRSwNP, but the difference was not significant. In nasal polyp tissue, there is a significant difference in TGF-β1 and IL-8 expression between CRSwNP and recurrent CRSwNP, where the expression of both cytokines is lower in recurrent CRSwNP. Interleukin-5 expression was higher in recurrent CRSwNP than CRSwNP, but the difference was not significant. In the polyps mucosal, IL-5 has the main role in recurrent CRSwNP polyp, whereas TGF-β has the main role in polyp tissue. CONCLUSION: This study concluded that the expression of IL-5 in the mucosa could be examined with simple techniques like brushing before polypectomy or FESS was performed to determine the possibility of polyps recurrencies.

Longzuan Tongbi Formula (LZTB) is an effective proved prescription in Zhuang medicine for treating active rheumatoid arthritis (RA). However, its active ingredients, underlying targets, and pharmacological mechanism are still not clear in treating RA. We have applied network pharmacology to study LZTB and found that 8 herbs in LZTB and 67 compounds in the 8 herbs are involved in the regulation of RA-related genes; we have conducted pathway analysis of overlapping genes and found that 7 herbs participate in the regulations of 24 pathways associated with RA and that 5 herbs in the 7 herbs and 25 compounds in the 5 herbs participate in the regulation of hsa05323 (rheumatoid arthritis). The results indicated that all herbs in LZTB and some compounds in those herbs participate in the treatment of RA; 25 compounds are main active ingredients and hsa05323 (rheumatoid arthritis) is the major pathway in the treatment of RA. We have also found that three pathways (inflammatory mediator regulation of TRP channels, PPAR signaling pathway, and mTOR signaling pathway) might have some effect on the treatment of RA.

Inflammatory responses have a pivotal role in the development of diabetic nephropathy (DN). The nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome is a newly recognized and potent inflammatory mediator that induces inflammatory responses in several disorders, including DN. The suppression of procytokine release and inflammatory response is integral to the prevention of complications arising from the inflammatory process. In this review, we discuss the role of the NLRP3 inflammasome in the pathogenesis of DN, focusing on its effects on interleukin (IL)-1β and IL-18. Furthermore, we review the potential anti-inflammatory effects of antidiabetic drugs used in routine clinical practice, such as insulin, biguanides, Sodium-glucose co-transporter-2 (SGLT2) inhibitors, sulfonylureas, thiazolidinediones, and dipeptidyl peptidase-4 (DPP-4) inhibitors. In addition, we discuss whether these drugs can also modulate NLRP3 inflammasome activity in renal tissues.

Cell regenerative therapy is a modern solution for difficult-to-heal wounds. Keratinocytes, the most common cell type in the skin, are difficult to obtain without the creation of another wound. Stem cell differentiation towards keratinocytes is a challenging process, and it is difficult to reproduce in chemically defined media. Nevertheless, a co-culture of keratinocytes with stem cells usually achieves efficient differentiation. This systematic review aims to identify the secretions of normal human keratinocytes reported in the literature and correlate them with the differentiation process. An online search revealed 338 references, of which 100 met the selection criteria. A total of 80 different keratinocyte secretions were reported, which can be grouped mainly into cytokines, growth factors, and antimicrobial peptides. The growth-factor group mostly affects stem cell differentiation into keratinocytes, especially epidermal growth factor and members of the transforming growth factor family. Nevertheless, the reported secretions reflected the nature of the involved studies, as most of them focused on keratinocyte interaction with inflammation. This review highlights the secretory function of keratinocytes, as well as the need for intense investigation to characterize these secretions and evaluate their regenerative capacities. Funding Agencies|Centre for Advanced Medical Products, Sweden; Hand and Plastic Surgery Department, Linkoping University Hospital, Region Ostergotland, Sweden

Background The pathological conditions of UC and CD involved in inflammatory bowel disease-unclassified (IBD-U), UC with primary sclerosing cholangitis (PSC-UC), and UC with autoimmune pancreatitis type 2 (AIP-UC) remain unclear. Therefore, it is difficult to decide the appropriate treatments for these subtypes of UC. Our aim was to examine whether the discriminant equation using the mucosally expressed mediators designed as our previous study for IBD, could characterize IBD-U, PSC-UC, or AIP-UC. Methods A total of 56 patients including UC (n = 24), CD (n = 15), IBD-U (n = 10), PSC-UC (n = 4), and AIP-UC (n = 3), along with 9 control patients were enrolled in this study. Mucosally expressed inflammatory mediators related to Th1, Th2, Th17, and Treg were measured using quantitative PCR in endoscopic biopsies from the inflamed intestines of the patients. The IBD-U, PSC-UC or AIP-UC were characterized using discriminant analysis and principle component analysis. Results Through discriminant analyses, combinations of 3 to 7 inflammatory mediators were used to discriminate between UC and CD. Moreover, the identified 3 markers could diagnose patients with IBD-U as UC or CD with high accuracy. The distribution graph of inflammatory mediators using the principal component analysis revealed that PSC-UC and AIP-UC exhibited CD-like and UC-like features, respectively. Conclusions The discriminant equation using mucosally expressed mediators of IL-13, IL-21 and T-bet can be used as a universal diagnostic tool not only for IBD-U but also to assess pathological conditions in PSC-UC and AIP-UC.

Diabetic retinopathy (DR), the most common complication of diabetes mellitus, is associated with oxidative stress, nuclear factor-kB (NFkB) activation, and excess production of vascular endothelial growth factor (VEGF) and intracellular adhesion molecule-1 (ICAM-1). Current therapies are invasive, frequently ineffective, and have adverse effects. The application of far-red to near-infrared (NIR) light (630-1000nm) reduces oxidative stress and inflammation in vitro and in vivo. Thus, we hypothesize that 670nm light treatment will dimish oxidative stress preventing downstream inflammatory mechanisms associated with DR. We used an in vitro model system of rat Müller glial cells grown under normal (5 mM) or high (25 mM) glucose conditions and treated with a 670 nm light emitting diode array (LED) (4.5 J/cm2) or no light (sham) daily. We report that a single 670 nm light treatment diminished ROS production and preserved mitochondrial integrity and ATP production in this in vitro model of diabetic retinopathy. Furthermore, treatment for 3 days in culture reduced NFkB activity to levels observed in normal glucose and prevented the subsequent increase in ICAM-1. The ability of 670nm light treatment to prevent early molecular changes in this established DR model system suggests light treatment could become an early therapeutic option for DR.

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 is a global pandemic and poses a major threat to human health worldwide. In addition to respiratory symptoms, COVID-19 is usually accompanied by systemic inflammation and liver damage in moderate and severe cases. Nuclear factor erythroid 2-related factor 2 (NRF2) is a transcription factor that regulates the expression of antioxidant proteins, participating in COVID-19-mediated inflammation and liver injury. Here, we show the novel reciprocal regulation between NRF2 and inflammatory mediators associated with COVID-19-related liver injury. Additionally, we describe some mechanisms and treatment strategies.

An important trend in the personal care industry involves the development of body wash products that not only clean the skin without damage but deposit conditioning ingredients to improve skin barrier function.The objective of this study was to develop skin biomarker measures to quantify the treatment effects of body wash products.We employed analysis of structural proteins (keratin 1,10,11 and involucrin), a natural moisturizing factor (pyrrolidone carboxylic acid) and an inflammatory mediator (IL-1ra/IL-1α) from adhesive discs with dry skin grading, TEWL and capacitance measurements to compare the effects of direct application of petrolatum, a high petrolatum depositing body wash, and a regular body wash on dry leg skin in a standard leg-wash treatment protocol.High depositing body wash and petrolatum had positive effects on stratum corneum barrier function as judged by biomarker analysis, biophysical measurements and skin grading compared to the regular body wash product.The results clearly indicate that a combination of biomarker and biophysical property measurements is effective for determining the skin benefits of moisturizing body wash products.Une tendance importante dans l’industrie des soins personnels inclut le développement de produits de lavage corporel qui non seulement nettoient la peau sans l’endommager, mais déposent des ingrédients de traitement pour améliorer la fonction de la barrière cutanée.L’objectif de cette étude était de développer des mesures de biomarqueurs cutanés permettant de quantifier les effets du traitement des produits de lavage corporel. MÉTHODES: Nous avons utilisé l’analyse de protéines structurelles (kératine 1,10,11 et involucrine), un facteur hydratant naturel (acide carboxylique de pyrrolidone) et un médiateur inflammatoire (IL-1ra/IL-1a) provenant de disques adhésifs avec cotation de la sécheresse cutanée, mesures de perte d’eau transépidermique (transepidermal water loss, TEWL) et de capacitance pour comparer les effets de l’application directe de vaseline, d’un produit de lavage corporel avec dépôt élevé de vaseline et d’un produit de lavage corporel ordinaire sur la peau sèche des jambes, dans un protocole de traitement de lavage des jambes standard. RÉSULTATS: Le produit de lavage corporel à dépôt élevé et la vaseline avaient des effets positifs sur la fonction de barrière de la couche cornée, comme évalué par l’analyse des biomarqueurs, les mesures biophysiques et la cotation de la peau, comparé au produit de lavage corporel ordinaire.Les résultats indiquent clairement qu’une combinaison de mesures des biomarqueurs et des propriétés biophysiques est efficace pour déterminer les bienfaits pour la peau des produits de lavage corporel hydratants.

Background: Asian sand dust (ASD) and Aspergillus fumigatus are known risk factors for airway mucosal inflammatory diseases. Bacterial and fungal biofilms commonly coexist in chronic rhinosinusitis and fungus balls. We evaluated the effects of ASD on the development of A. fumigatus biofilm formation on nasal epithelial cells. Methods: Primary nasal epithelial cells were cultured with A. fumigatus conidia with or without ASD for 72 h. The production of interleukin (IL)-6, IL-8, and transforming growth factor (TGF)-β1 from nasal epithelial cells was determined by the enzyme-linked immunosorbent assay. The effects of ASD on A. fumigatus biofilm formation were determined using crystal violet, concanavalin A, safranin staining, and confocal scanning laser microscopy. Results: ASD and A. fumigatus significantly enhanced the production of IL-6 and IL-8 from nasal epithelial cells. By coculturing A. fumigatus with ASD, the dry weight and safranin staining of the fungal biofilms significantly increased in a time-dependent manner. However, the increased level of crystal violet and concanavalin A stain decreased after 72 h of incubation. Conclusions: ASD and A. fumigatus induced the production of inflammatory chemical mediators from nasal epithelial cells. The exposure of A. fumigatus to ASD enhanced the formation of biofilms. The coexistence of ASD and A. fumigatus may increase the development of fungal biofilms and fungal inflammatory diseases in the sinonasal mucosa.

Introduction: Nourin is an inflammatory mediator rapidly released by ischemic myocardium “before” necrosis, and by necrotic cells . It stimulates leukocyte “ chemotaxis ” and “ activates ” leukocytes and vascular endothelial cells to release several “ cytokine storm ” mediators. Using Nourin amino acid sequence, Bioinformatics analysis indicated that Nourin is likely regulated by miRNA-106b ; an inflammatory-signaling pathway linked to myocardial ischemia. Hypothesis: As an "initial" inflammatory marker, the Nourin-dependent miR-106b can early diagnose ischemia-induced injury in UA patients when Troponin levels are below the decision limit, and in STEMI patients. The underlying regulatory mechanism involves lncR-CTB89H12.4 and mRNA-ANAPC11; associated with ischemia. Methods: Gene expression of lncR-CTB89H12.4 / miR-106b and mRNA-ANAPC11 were measured in serum samples from UA (n=30 - confirmed by invasive coronary angiography and negative Troponin) and STEMI (n=16) patients at presentation, and healthy volunteers (n=16). Results: Gene expression of miR-106b was up-regulated by 150-fold in UA compared to healthy, and by 4.6-fold in STEMI compared to UA (Fig. 1). Receiving Operator Characteristics (ROC) analysis revealed a statistically significant difference in miR-106b that discriminated UA from healthy controls with a test sensitivity of 87% sensitivity & specificity of 88%. Diagnostic sensitivity was 86% and specificity was 90% for discriminating UA from STEMI. Additionally, Spearman’s correlation analysis revealed a significant association of miR-106b with lncR-CTB89H12.4 and mRNA-ANAPC11. The down regulation of lncR-CTB89H12.4 after ischemia resulted in the up-regulation of miR-106b and activation of mRNA-ANAPC11 . Conclusions: The Nourin-dependent miR-106b is a promising early inflammatory biomarker indicating UA patients and discriminating between UA and STEMI. Regulations appears to be from lncR-CTB89H12.4 and mRNA-ANAPC11 .

Introduction: No blood biomarker exits that can diagnose Unstable Angina (UA) patients. Nourin is ischemia-dependent inflammatory mediator rapidly released by reversible ischemic myocardium “before” necrosis, and by necrotic cells. Using Nourin amino acid sequence, Bioinformatics analysis indicated that Nourin is likely regulated by miR-137; a marker of cell damage and a hypoxiaresponsive autophagy-signaling pathway linked to myocardial ischemia and coronary artery disease. Hypothesis: That the Nourin-dependent miR-137, is an early biomarker for UA patients when Troponin levels are below the decision limit. The underlying regulatory mechanism involves lncRCTB89H12.4 and mRNA-FTLH-17; also associated with ischemia. Methods: We measured serum gene expression profile of lnc-CTB89H12.4/miR-137 and mRNAFTHL- 17 in UA (n=30 - confirmed by invasive coronary angiography and negative Troponin) and STEMI (n=16) patients at presentation, and healthy volunteers (n=16). Results: Gene expression of miR-137 was up-regulated by 1,185-fold in UA (median=1,244.41) compared to healthy (1.05), and by 2.5-fold in STEMI (3,162.72) compared to UA (Fig. 1). Receiving Operator Characteristics (ROC) analysis revealed a statistically significant difference in miR-137 that discriminated UA from healthy controls with a test sensitivity & specificity of 96% & 93%, respectively. Diagnostic sensitivity was 75% & specificity was 83% for discriminating UA from STEMI. Additionally, Spearman’s correlation analysis revealed a significant association of miR-137 with lncRCTB89H12.4and mRNA-FTHL-17. The down-regulation of lncR-CTB89H12.4 after ischemia resulted in the up-regulation of miR-137 and activation of mRNA-FTLH-17. Conclusions: As a marker of cell damage, the Nourin-dependent miR-137 is a promising early diagnostic biomarker indicating UA patients and discriminating between UA and STEMI. Regulations appears to be from lncR-CTB89H12.4 and mRNA-FTLH-17.

Recent literature has highlighted the importance of chronic inflammation in psoriasis pathogenesis. Non-resolving inflammation can trigger progressive tissue damage and inflammatory mediator release which in turn perpetuate the inflammatory cycle. Under normal conditions, inflammatory responses are tightly controlled through several mechanisms that restore normal tissue function and structure. Defects in regulatory mechanisms of the inflammatory response can result in persistent unresolved inflammation and further increases of inflammation. Therefore, this review focuses on defects in regulatory mechanisms of inflammatory responses that lead to uncontrolled chronic inflammation in psoriasis. Databases such as Pubmed Embase, ISI, and Iranian databases including Iranmedex, and SID were researched to identify relevant literature. The results of this review indicate that dysregulation of the inflammatory response may be a likely cause of various immune-mediated inflammatory disorders such as psoriasis. Based on current findings, advances in understanding the cellular and molecular mechanisms involved in inflammation resolution are not only improving our knowledge of the pathogenesis of chronic inflammatory diseases but also supporting the development of new therapeutic strategies.

Nucleotide-binding domain, leucine-rich repeat receptors (NLRs) mediate innate immunity by forming inflammasomes. Activation of the NLR protein NLRP1 requires autocleavage within its function-to-find domain (FIIND)1–7. In resting cells, the dipeptidyl peptidases DPP8 and DPP9 interact with the FIIND of NLRP1 and suppress spontaneous NLRP1 activation8,9; however, the mechanisms through which this occurs remain unknown. Here we present structural and biochemical evidence that full-length rat NLRP1 (rNLRP1) and rat DPP9 (rDPP9) form a 2:1 complex that contains an autoinhibited rNLRP1 molecule and an active UPA–CARD fragment of rNLRP1. The ZU5 domain is required not only for autoinhibition of rNLRP1 but also for assembly of the 2:1 complex. Formation of the complex prevents UPA-mediated higher-order oligomerization of UPA–CARD fragments and strengthens ZU5-mediated NLRP1 autoinhibition. Structure-guided biochemical and functional assays show that both NLRP1 binding and enzymatic activity are required for DPP9 to suppress NLRP1 in human cells. Together, our data reveal the mechanism of DPP9-mediated inhibition of NLRP1 and shed light on the activation of the NLRP1 inflammasome., The 2:1 complex between the inflammatory mediator NLRP1 and the dipeptidyl peptidase DPP9 functions to sequester an inflammasome-forming fragment of NLRP1 and enhance NLRP1 autoinhibition.

There is limited information available regarding the association of plasma free fatty acids (FFA) and inflammation mediators with ischemic stroke. At the same time, new treatment strategies are being pursued. The aim of this study was to carry out a thorough analysis of inflammation with multiple FFA-derivative mediators after and ischemic stroke and standard treatment. HPLC separations of 17 eicosanoids were performed using an Agilent Technologies 1,260 liquid chromatograph. The profiles of the esters of fatty acids were labelled by means of gas chromatography. FFA, and eicosanoid profiles in the group of patients after ischemic stroke significantly differed from the profile of the control group. Studies confirmed the involvement of derivative synthesis pathways responsible for the inflammation, especially palmitic acid (9 and 13 HODE), arachidonic acid, EPA and DHA. Arachidonic acid derivatives were synthesised on 5LOX, 15 LOX and COX pathways with the participation of prostaglandins while omega 3 derivatives strengthened the synthesis of resolvins, RevD1 in particular. The ability to accelerate the quenching of inflammation after ischemic stroke seems to be a promising strategy of stroke treatment in its early stage. In this context, our study points to lipoxins, RevD1, and 9, 13 HODE as the most important derivatives.

Background Bovine mastitis is the inflammatory response of the mammary gland with an utmost threat to the dairy industry worldwide. Cytokine networks fuel inflammation. The sensitive and subtle changes of the inflammatory cytokine network in healthy and mastitic bovine mammary gland may encourage the use of cytokines in the diagnosis and prognosis of bovine mastitis. Allograft inflammatory factor-1 (AIF-1) is a proinflammatory cytokine mainly secreted by immune cells and it plays a central role in the complex signaling network of inflammation activation. Therefore, we explored the possible role of bovine AIF-1 related to bovine mastitis in the present study. Results The average concentration of AIF-1 in milks suffering from mastitis was 2.5 fold of that in the healthy cows, while its value decreased in cows recovered from mastitis. Furthermore, recombinant bovine AIF-1 up-regulated TNF-α, IL-6, and monocyte chemoattractant protein 1 secretion from bovine mammary epithelial cells with NF-κB activating, then NF-κB signaling inhibitor BAY 11-7085 abolished the increase of these inflammatory cytokines secretion induced by AIF-1. Thereafter, AIF-1 impaired bovine mammary epithelial cell viability, induced cell membrane permeability and cell apoptosis with exacerbated nitric oxide and oxidative stress, activated caspase 3, decreased mitochondrial membrane potential and intracellular ATP concentration. Conclusion These results indicated that AIF-1 prompted inflammation mediator production of bovine mammary epithelial cells via NF-κB signaling. Moreover, it damaged epithelial cells by depressing cell viability, inducing cell membrane permeability and cell apoptosis, which might be related to bovine mastitis.

Background and Aims The removal of inflammatory mediators and cytokines is of great importance in the treatment of patients with acute or chronic renal failure. In patients with acute renal failure and sepsis, an attempt is made to achieve removal through the use of high-volume treatments or adsorbers in order to achieve better circulatory stability. In chronic dialysis patients, this has so far not been sufficiently addressed, but is important for mortality and cardiovascular events (MIA syndrome). Some studies show a superiority of HDF over conventional HD. By using new MCO filters in HD mode such as the Baxter Theranova (HDx), an improvement of cytokine status seems to be possible in both areas (chronic and acute). The effectiveness of MCO filters (HDx) compared to high flux hemodiafiltration in the removal of interleukins (interleukin 6, interleukin 10 and TNF (tumor necrosis factor) alpha will be assessed. Method The efficacy of HDx was compared with that of conventional high-flux dialysis filters (Fresenius FX80, HDF) in HDF mode. Based on real world conditions the ultrafiltration/substitution rate was set to 50 ml/min. (blood flow 200 ml/min., dialysate flow 500 ml/min.) No effective ultrafiltration was used. The measurements were performed in vitro in a 3l pool of fresh frozen plasma (citrate anticoagulated, with additional heparin during dialysis treatment). IL6 (24.5 kDa) IL10 (18.6 kDa, dimer)) and TNFalpha (17.4 kDa, trimer) were added to the plasma pool in concentrations of 1.5 μg/l each. This results in very high cytokine levels, as for example in severe sepsis. Samples were taken before and after the dialyzer for 180 minutes (after 5, 15, 30, 60, 120 and 180 minutes).For HDF the measured cytokine concentration was corrected for ultrafiltration rates. In addition to cytokines, albumin and total protein concentration were measured (ELISA Kit LEGEND MAX Human IL-6 / IL-10 / TNF-α; Biolegend and Cobas Mira Plus; Roche Kit LT-AB 0103 and LT-TP 0253). Every test was repeat 5 times. Results Theranova HDx showed higher removal rates of all tested cytokines over a period of 180 minutes. A comparison of the concentrations at the beginning and end of the measurements showed: IL-6 reduction - HDx about 77% / HDF about 63%. IL-10 reduction - HDx about 53% and HDF about 22%. TNF-α Reduction - HDx about 26%; HDF about 18% The concentration of albumin and total serum protein was not significant different during the treatments in both groups. Conclusion Hemodialysis therapy with Theranova HDx appears to be a superior or equal therapy option for the removal of cytokines. This opens up new treatment options for both acute renal failure and chronic dialysis patients, especially if citrate anticoagulation is necessary. The ultrafiltration rate in HDF was lower than recommended for high volume diafiltration,but as high as in our real world experience. Therefore the effect of HDF could be underestimated. Clinical studies with clinically relevant blood flow and ultrafiltration rates are still necessary.

Aim: This cross-sectional case-control study evaluated the serum carnitine level in children with urinary tract infection (UTI). Background: Acute pyelonephritis (APN) is a common bacterial infection of the upper urinary tract in children which may also lead to renal damage and tubular atrophy. Activation of inflammatory mediator bedside alterations in the cytokines and generation of reactive oxygen species (ROS) play a striking role in the development of tissue damage after pyelonephritis. L-carnitine as one of the most potent natural antioxidant agents by inhibition of lipid peroxidation may protect cells and tissues from damage. Methods: A total of 30children with UTI (as a case group) and 30 healthy children (as a control group) which matched as age and sex were enrolled in this study. All children were evaluated and compared as age, sex, weight, body mass index (BMI) and serum carnitine level together. Serum carnitine level wasdetermined using serum carnitine ELISA kit. Results: Demographic and clinical data such as age, sex, weight and BMI were not statistically significant between two groups. The serum carnitine levels were significantly lower in case group with UTI than control group. Mean serum carnitine concentration in the case group and in control group was 36.56 ± 9.87 μmol/l and 62.8±21.35 respectively (P = 0.001). Conclusion: According to our study, it could be concluded that low serum L-carnitine level is linked to UTI in children. Therefore, further studies are needed to confirm our results.

[ES] Introducción La infección por el coronavirus SARS-CoV-2 originada en diciembre de 2019 en la región china de Wuhan ha adquirido proporciones pandémicas. A día de hoy ha ocasionado más de 1,7 millones de contagios y más de 100.000 muertes en todo el mundo. La investigación científica actual se centra en el mejor conocimiento de la infección aguda y de sus estrategias terapéuticas. Dada la magnitud de la epidemia, planteamos una revisión especulativa sobre las posibles consecuencias en patología neurológica a medio/largo plazo, con especial atención a enfermedades neurodegenerativas y neuropsiquiátricas con base neuroinflamatoria, teniendo en cuenta la evidencia directa de afectación neurológica a causa de la infección aguda. Desarrollo Revisamos de forma sistemática lo conocido sobre los mecanismos patogénicos de la infección por SARS-CoV-2, la repercusión de la tormenta de citoquinas sobre el sistema nervioso central y su persistencia en el tiempo y las consecuencias que la neuroinflamación puede tener sobre el sistema nervioso central. Conclusiones El SARS-CoV-2 es un virus neuroinvasivo capaz de provocar una tormenta de citoquinas que podría convertirse en persistente en población seleccionada. Aunque nuestra hipótesis tiene alto componente especulativo, la repercusión que esta situación puede tener en la puesta en marcha y progresión de enfermedades neurodegenerativas y neuropsiquiátricas con base neuroinflamatoria debe ser considerada como posible germen de una pandemia demorada que podría tener un gran impacto en salud pública a medio o largo plazo. Se hace necesario un estrecho seguimiento de la salud cognitiva y neuropsiquiátrica de los pacientes supervivientes a infección COVID-19., [EN] Introduction SARS-CoV-2 was first detected in December 2019 in the Chinese city of Wuhan and has since spread across the world. At present, the virus has infected over 1.7 million people and caused over 100 000 deaths worldwide. Research is currently focused on understanding the acute infection and developing effective treatment strategies. In view of the magnitude of the epidemic, we conducted a speculative review of possible medium- and long-term neurological consequences of SARS-CoV-2 infection, with particular emphasis on neurodegenerative and neuropsychiatric diseases of neuroinflammatory origin, based on the available evidence on neurological symptoms of acute SARS-CoV-2 infection. Development We systematically reviewed the available evidence about the pathogenic mechanisms of SARS-CoV-2 infection, the immediate and lasting effects of the cytokine storm on the central nervous system, and the consequences of neuroinflammation for the central nervous system. Conclusions SARS-CoV-2 is a neuroinvasive virus capable of triggering a cytokine storm, with persistent effects in specific populations. Although our hypothesis is highly speculative, the impact of SARS-CoV-2 infection on the onset and progression of neurodegenerative and neuropsychiatric diseases of neuroinflammatory origin should be regarded as the potential cause of a delayed pandemic that may have a major public health impact in the medium to long term. Cognitive and neuropsychological function should be closely monitored in COVID-19 survivors.

Zika virus (ZIKV) is an emergent arthropod-borne virus whose outbreak in Brazil has brought major public health problems. Infected individuals have different symptoms, including rash and pruritus, which can be relieved by the administration of antiallergics. In the case of pregnant women, ZIKV can cross the placenta and infect the fetus leading to congenital defects. We have identified that mast cells in the placentae of patients who had Zika during pregnancy can be infected. This led to our investigation on the possible role of mast cells during a ZIKV infection, using the HMC-1 cell line. We analyzed their permissiveness to infection, release of mediators and ultrastructural changes. Flow cytometry detection of ZIKV-NS1 expression 24 h post infection in 45.3% of cells showed that HMC-1 cells are permissive to ZIKV infection. Following infection, &beta, hexosaminidase was measured in the supernatant of the cells with a notable release at 30 min. In addition, an increase in TNF-&alpha, IL-6, IL-10 and VEGF levels were measured at 6 h and 24 h post infection. Lastly, different intracellular changes were observed in an ultrastructural analysis of infected cells. Our findings suggest that mast cells may represent an important source of mediators that can activate other immune cell types during a ZIKV infection, which has the potential to be a major contributor in the spread of the virus in cases of vertical transmission.

Background Rheumatic fever has a marked tendency to recur leading to high risk of chronic heart lesions or worsening lesions in patients with previous rheumatic heart disease. For secondary prevention of RF, long acting penicillin can be used. Some rheumatic heart disease patients suffer from atrial fibrillation. Cardiac rhythm may affect the response of the body to the long acting penicillin, so it would be helpful to study the effect of cardiac rhythm on serum levels of inflammatory mediators in patients with chronic rheumatic heart disease. Objectives Our study is a prospective cross-sectional controlled study that aims to study the effect of cardiac rhythm on serum levels of the inflammatory mediators; C-Reactive Protein and Interleukin-6 in patients with chronic rheumatic heart disease. Methods The study included 70 rheumatic heart disease patients on regular long acting penicillin. Patients were divided into to 2 groups: Group A; 56 patients with rheumatic heart disease who have sinus rhythm, and Group B; 14 patients with rheumatic heart disease who have atrial fibrillation (AF) and Group C; control group of 10 healthy individuals. Results There was no significant difference between sinus patients and AF patients in CRP and IL-6 levels (p = 0.3050 and 0.6758, respectively). Also, there was no significant difference between 15, 21 and 30 days regimens of penicillin in CRP and IL-6 levels (p = 0.9467and 0.0795, respectively). IL6 values were significantly correlated with CRP values (r = 0.5435, p Conclusion Our study results disprove that cardiac rhythm has an effect on the serum levels of the inflammatory mediators C-Reactive Protein and Interleukin-6 in chronic rheumatic heart disease. Our study also disproves the preference of any regimen of long acting penicillin (15 days, 21 days and 30 days) over each other for secondary prevention of chronic rheumatic heart disease. Our study results emphasized that chronic rheumatic heart disease is an inflammatory process mediated with some mediators as CRP and IL-6 that are strongly correlated with each other.

Background: Infants after cardiopulmonary bypass are exposed to increasing inflammatory mediator release and are at risk of developing fluid overload. The aim of this pilot study was to evaluate the impact of passive peritoneal drainage on achieving negative fluid balance and its ability to dispose of inflammatory cytokines. Methods: From September 2014 to November 2016, infants undergoing STAT category 3, 4, and 5 operations were randomized to receive or not receive intraoperative prophylactic peritoneal drain. We analyzed time to negative fluid balance and perioperative variables for each group. Pro- and anti-inflammatory cytokines were measured from serum and peritoneal fluid in the passive peritoneal drainage group and serum in the control group postoperatively. Results: Infants were randomized to prophylactic passive peritoneal drain group (n = 13) and control (n = 12). The groups were not significantly different in pre- and postoperative peak lactate levels, postoperative length of stay, and mortality. Peritoneal drain patients reached time to negative fluid balance at a median of 1.42 days (interquartile range [IQR]: 1.00-2.91), whereas the control at 3.08 (IQR: 1.67-3.88; P = .043). Peritoneal drain patients had lower diuretic index at 72 hours, median of 2.86 (IQR: 1.21-4.94) versus 6.27 (IQR: 4.75-11.11; P = .006). Consistently, tumor necrosis factor-α, interleukin (IL)-4, IL-6, IL-8, IL-10, and interferon-γ were present at higher levels in peritoneal fluid than serum at 24 and 72 hours. However, serum cytokine levels in peritoneal drain and control group, at 24 and 72 hours postoperatively, did not differ significantly. Conclusions: The prophylactic passive peritoneal drain patients reached negative fluid balance earlier and used less diuretic in early postoperative period. The serum cytokine levels did not differ significantly between groups at 24 and 72 hours postoperatively. However, there was no significant difference in mortality and postoperative length of stay.

Introduction: Nonsteroidal anti-inflammatory drugs (NSAIDs) intervene in the COX (cyclooxygenase) pathways which generate two important inflammation mediators, prostaglandins (PGs) and leukotriene ...