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Neuropathic pain (NeP) is a type of persistent pain initiated by diseases or injuries of the nervous system. Although the underlying pathophysiological mechanisms of NeP are poorly understood, the immune system plays a key role in this condition. M2 macrophages have a key role in tissue healing and the reduction of inflammation. This systematic study aims to provide an overview of the role and importance of M2 macrophages in NeP after spinal cord injury (SCI). A comprehensive systematic review was conducted utilizing Scopus, PubMed, Embase, and ISI Web of Science databases. Two independent reviewers conducted the article selection. All publications examine the impact of M2 macrophages on NeP following spinal cord injuries. A quality assessment was conducted on bias entities that had been predetermined. Eleven papers met the criteria. According to the findings, focusing on immune cell polarization presents viable therapeutic options for treating NeP and enhancing recovery after SCI. M2 macrophages are essential for reducing neuropathic pain and promoting recovery after spinal cord injury. The modulation of M2 macrophages by a number of therapeutic approaches, including ivermectin-functionalized MWCNTs, isorhamnetin, Neuregulin-1 administration, TMEM16F inhibition, lentivirus-mediated delivery of anti-inflammatory cytokines, epigallocatechin-3-gallate, and red-light therapy promotes neuroregeneration, decreases neuroinflammatory cytokines, and reduces NeP. The results of these preclinical investigations must, however, be interpreted with caution, according to the quality assessment and risk of bias analysis of the studies that were included. Targeting M2 macrophages may have therapeutic benefits as they are essential for the management of NeP and recovery following spinal cord damage. Keywords: Neuropathic pain, Spinal cord, Injury, Macrophage, Anti-inflammatory, Allodynia, Author(s): Aidin Shahrezaei[sup.1], Maryam Sohani[sup.1], Mohammadhassan Sohouli[sup.2], Soroush Taherkhani[sup.3] and Farinaz Nasirinezhad[sup.3,4,5] Introduction Neuropathic pain (NeP) is pain that occurs due to structural or functional issues with the nervous system [...]

Context: Pollution-related health hazards are very common among people living and/or working in industrial areas, particularly near industries and metro cities. These air pollutants contribute to allergens, increase inflammation, and affect lung function. Aim: The present study aimed to examine the effect of yoga training on lung functions and inflammation in terms of soluble interleukin-2 receptor (sIL-2R) in people working and living in a polluted area. Settings and Design: This is a randomized controlled interventional pilot study. Methods and Materials: Forty-eight male volunteers from the industrial area, aged 20-50 years, were randomly assigned to the experimental group and the control group. Each group comprises 24 study participants. Lung function and sIL-2R were studied at the baseline and post-yoga intervention period of 16 weeks. Statistical Analysis Used: Study data were analyzed using descriptive methods, a one-tailed t-test, a paired t-test, and an independent t-test. Result: Study results showed directional and significant improvements in forced vital capacity, forced expiratory volume in the first second, and peak expiratory flow rate compared to the control group participants. The results pertaining to sIL-2R showed a directional and significant decrease in the experimental group compared to the control group. Conclusion: The present study showed that yoga helps to promote better health, improve lung function and reduce inflammation among people residing in polluted environments. Keywords: Air pollutants, inflammation, lung function, sIL-2R, yoga, Author(s): Pratibha H. Rajbhoj (corresponding author) [1]; Satish D. Pathak [1]; Sucheta N. Patil [2] INTRODUCTION Industrial areas and metro cities of developing and developed countries are highly polluted zones. [...]

Background High-altitude exposure can cause oxidative stress damage in the intestine, which leads to increased intestinal permeability and bacterial translocation, resulting in local and systemic inflammation. Control of infection is critically dependent on the host's ability to kill pathogens with reactive oxygen species (ROS). Myeloperoxidase (MPO) targets ROS in pathogens. This study aimed to investigate the effects of hypoxia on the colonic mucosal barrier and myeloperoxidase (MPO)-mediated innate immune response in the colon. Methods and Results Genetically engineered mice were exposed to a hypobaric oxygen chamber for 3 days and an inflammation model was established using Salmonella Typhimurium infection. We found that hypoxic exposure caused the development of exacerbated bacterial colitis and enhanced bacterial dissemination in MPO-deficient mice. Infection and disease severity were associated with significantly increased Ly6G.sup.+ neutrophil and F4/80.sup.+ macrophage counts in infected tissues, which is consistent with elevated proinflammatory cytokines and chemoattractant molecules. Hypoxia restrained antioxidant ability and MPO deficiency aggravated the respiratory burst in the colon. Conclusion Hypoxia can damage the colonic mucosa. MPO mediates the innate immune response and regulates the mucosal and systemic inflammatory responses to Salmonella infection during hypoxia. Keywords: Hypoxia, Myeloperoxidase, Intestinal mucosa, Oxidative stress, Inflammation, Salmonella Typhimurium, Author(s): Qinfang Zhu[sup.1], Ying Han[sup.1], Xiaozhou Wang[sup.1], Ruhan Jia[sup.1], Jingxuan Zhang[sup.1], Meiheng Liu[sup.1] and Wei Zhang[sup.1] Background Gastrointestinal (GI) problems are common at high altitudes, and diarrhea is frequently observed, [...]

Application of cisplatin (CP) for the treatment of different cancers is known to cause pancreatitis through an increase in reactive oxygen species production and promotion of inflammation. Caffeic acid phenethyl ester (CAPE), the main activity carrier of propolis extracts, was previously found to possess numerous beneficial properties. This study aims to determine for the first time the potential of CAPE in preventing CP-induced pancreatic tissue damage by studying the changes occurring on both biochemical and microscopic levels. The levels of serum a-amylase and a panel of pancreatic tissue biomarkers related to tissue injury (reduced glutathione, xanthine oxidase, malondialdehyde, and protein carbonylated concentration) and inflammation (myeloperoxidase, nitric oxide, and umor necrosis factor alpha) were studied in male Wistar rats treated with either CP alone or with CP and CAPE. Additionally, microscopic analysis of pancreatic tissue would be conducted as well. Application of CAPE together with CP statistically significantly prevented the disturbance in all here-studied pancreatic tissue damage and inflammation-related biomarkers. The changes in pancreas biochemical status was followed by morphological disturbance. The results of the present study suggest that CAPE could act as a protective agent in pancreatic damage that arises after CP application. Key words: cisplatin, pancreatic damage, caffeic acid phenethyl ester, reactive oxygen species. On sait que l'application du cisplatine (CP) dans le traitement de differents cancers entraine des pancreatites par l'intermediaire d'une augmentation de la production de derives reactifs de l'oxygene et la promotion de l'inflammation. On a montre precedemment que l'ester phenylethylique de l'acide cafeique (ou CAPE pour[much less than] caffeic acid phenethyl ester[much greater than]), principal transporteur actif des extraits de propolis, est dote de nombreuses proprietes avantageuses. Cette etude visait a etablir pour la premiere fois le potentiel du CAPE dans la prevention des dommages que le CP entraine dans le tissu pancreatique, a l'aide de l'etude des changements survenant aux niveaux biochimique comme microscopique. Nous avons etudie les taux d'a amylase serique et un panel de biomarqueurs du tissu pancreatique lies aux lesions tissulaires (glutathion, xanthine oxydase, malondialdehyde et proteines carbonylees) et a l'inflammation (myeloperoxydase, oxyde nitrique et facteur de necrose tumorale alpha) chez des rats Wistar males auxquels etait administre du CP seul ou du CP avec du CAPE. Nous avons aussi mene une analyse microscopique du tissu pancreatique. L'application de CAPE avec du CP a permis de prevenir de maniere statistiquement significative les perturbations quant a tous les dommages du tissu pancreatique etudie ici et aux biomarqueurs lies a l'inflammation. Par ailleurs, les variations de l'etat biochimique du pancreas etaient suivies de perturbations morphologiques. Les resultats de la presente etude laissent entendre que le CAPE pourrait agir en tant qu'agent protecteur contre les dommages pancreatiques qui surviennent apres l'application de CP. [Traduit par la Redaction] Mots-cles: cisplatine, dommages pancreatiques, ester phenylethylique de l'acide cafeique, derives reactifs de l'oxygene., Introduction Cisplatin (CP) is one of the most renowned chemotherapeutic agents that have found their application in the treatment of head and neck, lung, testis, ovary, and breast cancers (Duan [...]

Background/Objectives We examined the prevalence of anaemia, iron deficiency, and inflammation during pregnancy and their associations with adverse pregnancy and infant outcomes in India. Subjects/Methods Three hundred and sixty-six women participating in a randomised trial of vitamin B.sub.12 supplementation were monitored to assess haemoglobin (Hb), serum ferritin (SF), hepcidin, C-reactive protein (CRP), and alpha-1-acid glycoprotein (AGP) during pregnancy. Women received vitamin B.sub.12 supplementation (50 [micro]g per day) or placebo daily; all women received daily prenatal iron-folic acid supplementation. Binomial and linear regression models were used to examine the associations of maternal iron biomarkers with pregnancy and infant outcomes. Results Thirty percent of women were anaemic (Hb < 11.0 g/dl), 48% were iron deficient (SF < 15.0 [micro]g/l), and 23% had iron deficiency anaemia at their first prenatal visit. The prevalence of inflammation (CRP > 5.0 mg/l: 17%; AGP > 1.0 g/l: 11%) and anaemia of inflammation (Hb < 11.0 g/dl, SF > 15.0 [micro]g/l, plus CRP > 5.0 mg/l or AGP > 1.0 g/l: 2%) were low. Infants born to anaemic women had a twofold higher risk of low birth weight ( Conclusions The prevalence of anaemia and iron deficiency was high early in pregnancy and associated with increased risk of adverse pregnancy and infant outcomes. A comprehensive approach to prevent anaemia is needed in women of reproductive age, to enhance haematological status and improve maternal and child health outcomes., Author(s): Julia L. Finkelstein [sup.1] [sup.2], Anura V. Kurpad [sup.2] [sup.3], Beena Bose [sup.2], Tinku Thomas [sup.2], Krishnamachari Srinivasan [sup.3], Christopher Duggan [sup.2] [sup.4] Author Affiliations: (1) Division of Nutritional [...]

Deep vein thrombosis (DVT), caused by alterations in venous homeostasis, is the third most common cause of cardiovascular mortality, however, key molecular determinants in venous thrombosis have not been fully elucidated. Several lines of evidence indicate that DVT occurs at the intersection of dysregulated inflammation and coagulation. The enzyme ectonucleoside tri(di)phosphohydrolase (ENTPD1, also known as CD39) is a vascular ecto-apyrase on the surface of leukocytes and the endothelium that inhibits intravascular inflammation and thrombosis by hydrolysis of phosphodiester bonds from nucleotides released by activated cells. Here, we evaluated the contribution of CD39 to venous thrombosis in a restricted-flow model of murine inferior vena cava stenosis. CD39 deficiency conferred a greater than 2-fold increase in venous thrombogenesis, characterized by increased leukocyte engagement, neutrophil extracellular trap formation, fibrin, and local activation of tissue factor in the thrombotic milieu. This venous thrombogenesis was orchestrated by increased phosphorylation of the p65 subunit of NF-[kappa]B, activation of the NLR family pyrin domain-containing 3 (NLRP3) inflammasome, and IL-1[beta] release in CD39-deficient mice. Substantiating these findings, an IL-1[beta]-neutralizing antibody or the IL-1 receptor inhibitor anakinra attenuated the thrombosis risk in CD39- deficient mice. These data demonstrate that IL-1[beta] is a key accelerant of venous thrombo-inflammation, which can be suppressed by CD39. CD39 inhibits in vivo crosstalk between inflammation and coagulation pathways and is a critical vascular checkpoint in venous thrombosis., Introduction The cell-surface enzyme ectonucleoside tri(di)phosphohydrolase-1 (ENTPD1), also known as CD39), is a key molecular factor protecting blood fluidity at the vessel-wall interface by catalyzing the hydrolytic cleavage of phosphodiester [...]

Purpose Mild therapeutic hypothermia (TH) is recommended as soon as possible after the return of spontaneous circulation to improve outcomes after out-of-hospital cardiac arrest (OHCA). Preclinical data suggest that the benefit of TH could be increased if treatment is started during cardiac arrest. We aimed to study the impact of intra-arrest therapeutic hypothermia (IATH) on neurological injury and inflammation following OHCA. Methods We conducted a 1:1 randomized, multicenter study in three prehospital emergency medical services and four critical care units in France. OHCA patients, irrespective of the initial rhythm, received either an infusion of cold saline and external cooling during cardiac arrest (IATH group) or TH started after hospital admission (hospital-cooling group). The primary endpoint was neuron-specific enolase (NSE) serum concentrations at 24 h. Secondary endpoints included IL-6, IL-8, and IL-10 concentrations, and clinical outcome. Results Of the 245 patients included, 123 were analyzed in the IATH group and 122 in the hospital-cooling group. IATH decreased time to reach temperature [less than or equal to]34 °C by 75 min (95 % CI: 4; 269). The rate of patients admitted alive to hospital was not different between groups [IATH n = 41 (33 %) vs. hospital cooling n = 36 (30 %); p = 0.51]. Levels of NSE and inflammatory biomarkers were not different between groups [median NSE at 24 h: IATH 96.7 [mu]g/l (IQR: 49.9-142.8) vs. hospital cooling 97.6 [mu]g/l (IQR: 74.3-142.4), p = 0.64]. No difference in survival and cerebral performance were found at 1 month. Conclusions IATH did not affect biological markers of inflammation or brain damage or clinical outcome., Author(s): Guillaume Debaty [sup.1] [sup.2], Maxime Maignan [sup.1] [sup.2], Dominique Savary [sup.3], François-xavier Koch [sup.2], Stéphane Ruckly [sup.4] [sup.12], Michel Durand [sup.5], Julien Picard [sup.5], Christophe Escallier [sup.2], Renaud Chouquer [...]

Previous studies have demonstrated that zymosan, a cell wall component of the yeast Saccharomyces cerevisiae, induces inflammation in experimental models. However, few studies have evaluated the potential of zymosan to induce sickness behavior, a central motivational state that allows an organism to cope with infection. To determine whether zymosan administration results in sickness behavior, mice were submitted to the forced swim (FST) and open field (OFT) tests 2, 6, and 24 h after treatment with zymosan (1, 10, or 100 mg/kg). Additionally, to evaluate the possible relationship between zymosan-induced sickness behavior and prostaglandin synthesis, mice were pretreated with the cyclooxygenase inhibitors indomethacin (10 mg/kg) and nimesulide (5 mg/kg) and the glucocorticoid drug dexamethasone (1 mg/kg). Zymosan induced time-dependent decreases in locomotor activity in the OFT, and an increase in immobility in the FST, and increased plasma levels of corticosterone at 2 h. Pretreatment with indomethacin, nimesulide, or dexamethasone blocked zymosan-induced behavioral changes in both the FST and OFT at 2 h post administration. These findings confirm previous observations that zymosan induces sickness behavior. Furthermore, our results provide new evidence that prostaglandin synthesis is necessary for this effect, as anti-inflammatory drugs that inhibit prostaglandin synthesis attenuated zymosan-induced behavioral changes. Keywords: Cyclooxygenase, Fungal infection, Prostaglandin, Saccharomyces cerevisiae, Sickness behavior, Zymosan, Author(s): Juliana B. M. Lima[sup.1], Clarice C. Veloso[sup.2], Fabiana C. Vilela[sup.2] and Alexandre Giusti-Paiva[sup.2] Introduction Physiological and behavioral changes induced by infection and inflammation can be induced in experimental animals [...]