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Objective: This work was implemented to elucidate the miR‐126‐5p expression in the plasma of patients with sepsis‐induced acute lung injury (ALI) and its correlation with inflammation and immune function. Methods: The peripheral blood of patients with sepsis‐induced ALI was obtained, and the levels of inflammatory factors (interleukin‐6 [IL‐6], C‐reactive protein [CRP], and procalcitonin [PCT]) were determined. Meanwhile, T lymphocyte subsets (CD3+, CD4+, and CD8+), and immunoglobulins (IgA, IgM, and IgG) were tested. miR‐126‐5p and TRAF6 mRNA expression in plasma was assessed. Receiver operating characteristic (ROC) curve was performed to assess the diagnostic accuracy of miR‐126‐5p in sepsis without ALI and sepsis with ALI. Correlation between miR‐126‐5p expression and clinical indicators was analyzed. The targets of miR‐126‐5p were predicted using the bioinformatics method, and the direct targets were verified through investigations. Results: miR‐126‐5p expression in plasma of patients with sepsis‐induced ALI was reduced than that of patients with sepsis without ALI. miR‐126‐5p expression was negatively correlated with IL‐6, CRP, and PCT but positively correlated with IgA, IgM, and IgG as well as CD3+, CD4+, and CD8+ in patients with sepsis‐induced ALI. ROC curve suggested that miR‐126‐5p (AUC: 0.777; 95%CI: 0.689–0.866) could distinguish patients with sepsis with ALI from patients with sepsis without ALI. TRAF6 expression in patients with sepsis‐induced ALI was higher than that in patients with sepsis without ALI. TRAF6 was a target gene of miR‐126‐5p, Conclusion: This research highlights that miR‐126‐5p is reduced in the plasma of patients with sepsis‐induced ALI, and miR‐126‐5p relates to systemic inflammation and immune function indicators. [ABSTRACT FROM AUTHOR]

Introduction: Environmental factors play a role in pathogenesis of both type 1 diabetes and atopic disease but they remain incompletely understood. T cell-mediated responses primarily of the T helper type 1 (Th1) are involved in type 1 diabetes while T helper type 2 (Th2) responses favour allergic disease. This TH 1/TH 2 paradigm is currently the source of much controversy in various studies. Objective: The aim of the study was to compare the reported country incidence of type 1 diabetes with the prevalence of atopic disease. Methods: The prevalence of wheeze, rhinitis, rhinoconjunctivitis and atopic eczema in the preceding 12 months in the 13- to 14-year-old age group was taken from The International Study of Asthma and Allergies in Childhood phase 1 study. These were compared to the age specific incidence of type 1 diabetes in children per 100 000 per year obtained from the Diabetes Mondiale Project Group study from those countries participating in both studies. Data collected from these 31 countries together with latitude was analysed using a Pearson correlation and significance analysis. A multiple regression analysis determined the confounding effect of latitude. Results: The incidence of type 1 diabetes was found to have a positive correlation with both wheezing ( P = 0.009) and atopic eczema ( P < 0.01). There was a no correlation between the incidence of type 1 diabetes and the prevalance of rhinitis (r = 0.02, P = 0.88) or of rhinoconjunctivitis (r = 0.026, P = 0.88). Latitude correlated negatively with type 1 diabetes and positively with rhinitis and rhinoconjnctuvits; it was not significantly correlated with wheeze or eczema. Regression analysis showed that latitude is a significant confounding factor in the correlation of rhinitis ( P value <0.0008) and rhinoconjunctivitis ( P value <0.0003) with diabetes. Conclusions: The study suggests that common environmental and/or genetic factors predispose to type 1 diabetes, wheezing and atopic eczema while factors predisposing to rhinitis and rhinoconjunctivitis appear to be distinct from those predisposing to type 1 diabetes. Please cite this paper as: Fsadni P, Fsadni C, Fava S and Montefort S. Correlation of worldwide incidence of type 1 diabetes (DiaMond) with prevalence of asthma and atopic eczema (ISAAC). Clin Respir J 2012; 6: 18-25. [ABSTRACT FROM AUTHOR]

Sarcoidosis is a multisystem granulomatous disease of unknown origin. Pathogenetic involvement of Mycobacterium tuberculosis has frequently been discussed in the aetiology of sarcoidosis; however, studies still remain contradictory. We addressed the question of mycobacterial involvement in the pathogenesis of sarcoidosis by analysing cellular immune responses to mycobacterial antigens. We examined the interferon (IFN)-γ production by enzyme-linked immunospot in response to purified protein derivate (PPD) mycobacterial-specific antigen early secretory antigenic target (ESAT)-6 and culture filtrate protein (CFP)-10 by peripheral blood mononuclear cells (PBMCs) and bronchoalveolar-lavage mononuclear cells (BALMCs) of patients with pulmonary sarcoidosis, smear-negative tuberculosis and controls. Release of IFN-γ in response to ex vivo contact with PPD, ESAT-6 or CFP-10 by BALMC and PBMC were comparable among patients with sarcoidosis and controls (PBMC P = 0.2326; BALMC P = 0.1767) and were less frequently observed in both groups compared to patients with tuberculosis (BALMC P < 0.05; PBMC P < 0.0001). Within PBMC, the immunophenotype of sarcoidosis patients differed from that of patients with tuberculosis, as well as from that of controls, while within BALMC it resembled that of patients with tuberculosis. In contrast to patients with tuberculosis, the frequency of mycobacteria-specific local and systemic immune responses is not elevated in patients with sarcoidosis when compared to controls. The immunophenotype represents the local resemblance of the granulomatous reaction underlying tuberculosis and sarcoidosis while showing systemical difference. These observations do not support a role of an infection with M. tuberculosis in the pathogenesis of sarcoidosis. Please cite this paper as: Hörster R, Kirsten D, Gaede KI, Jafari C, Strassburg A, Greinert U, Kalsdorf B, Ernst M and Lange C. Antimycobacterial immune responses in patients with pulmonary sarcoidosis. The Clinical Respiratory Journal 2009; 3: 229-238. [ABSTRACT FROM AUTHOR]

Abstract: Introduction: In the pathogenesis of asthma, an imbalance between helper T (Th) 1/Th2 and Th17/Treg cells is believed to play a key role in asthmatic inflammatory responses. Some studies indicated that zinc deficiency increases inflammatory factor production and worsens asthma. However, the effects of zinc on T cell profiles to reduce inflammatory response remain unclear. Objectives: We investigated the beneficial effects of zinc on isolated cell populations and cytokine levels from patients with asthma. Methods: Thirty‐six individuals Dermatophagoides pteronyssinus (Der p)‐allergic and 31 healthy subjects were enrolled in the study, and peripheral blood mononuclear cells (PBMCs) were collected. Harvested PBMCs were stimulated with recombinant Der p antigen in the presence or absence of zinc sulfate (25 μM or 50 μM) for 48 h. Cell surface markers and intracellular cytokine levels were examined by flow cytometry. The pro‐inflammatory factors in plasma and culture supernatants were measured by commercial enzyme‐linked immunosorbent assay. Results: Zinc sulfate dramatically reduced the proportions of Th2 and Th17 cells, but increased that of Th1 and Treg cells. Zinc sulfate also markedly reduced the levels of interleukin (IL)‐4 and IL‐17, but increased the levels of IFN‐γ. Conclusions: Zinc ameliorates the imbalance in T cell profiles and could be a potential adjuvant therapy for Der p‐induced allergic hypersensitivity. [ABSTRACT FROM AUTHOR]

Abstract: Introduction: B7‐H4, a member of the inhibitory B7 family, can restrain T cell proliferation, activation, cytokine secretion, and may be involved in immune evasion in cancer patients. Objectives: This aim of the study was to determine the expression level of soluble B7‐H4 (sB7‐H4) in circulation and to subsequently evaluate the clinical significance of circulating sB7‐H4 in patients with non‐small cell lung cancer (NSCLC). Methods: Serum specimens from 128 patients with NSCLC, 100 healthy volunteers (HV), and 80 patients with benign lung diseases (BLD) were collected. The concentrations of sB7‐H4 were measured by sandwich enzyme‐linked immunosorbent assay. Results: Serum sB7‐H4 levels in patients with NSCLC were significantly higher than those in patients with BLD (P < 0.05), or those in HV (P < 0.05). Using a cutoff of 27.8 ng/mL, the sensitivity and specificity of sB7‐H4 in differentiating between patients with NSCLC and patients with BLD, and between patients with NSCLC and HV was, 46.9% and 92.5%, and 54.7% and 95.0%, respectively. An area under the curve (AUC) for NSCLC resulting from sB7‐H4 (0.863), which was significantly better than any other tumour markers tested including CA125 (0.763), and CEA (0.775). Conclusion: In conclusion, assessment of serum sB7‐H4 levels could be considered as a diagnostic biomarker for NSCLC. [ABSTRACT FROM AUTHOR]

Background and Aims Helminths and their products are considered to possess therapeutic capability to control or even prevent immune-mediated diseases. Studies suggest that helminths induce a systemic immunomodulatory network, including regulatory T cells and anti-inflammatory interleukin-10 ( IL-10), which might play a key role in the protection against the allergic phenotype. Thus, helminthic therapy is becoming of a major interest, and several researchers are enthusiastically tended to explore its role in allergic diseases. Methods Peripheral blood mononuclear cells ( PBMCs) from 25 asthmatic and 25 healthy human were collected. After isolation of PBMCs, they were stimulated with excretory/secretory ( ES) antigen of M . marshalli, in incubator with 5% CO2, 37° C. Total RNA was isolated from all cells from antigen stimulated and non-stimulated control PBMC in asthmatic and healthy human after 6 h. The concentration of Th1 type cytokines [interferon-γ ( IFN-γ)] and Th2 type cytokines ( IL-4) and T-reg cytokines [transforming growth factor-β ( TGF-β), IL-10] was determined using real-time polymerase chain reaction. Results Results showed that the IFN-γ expression was significantly decreased in culture condition with ES Ag of M . marshalli in healthy and asthmatic patients ( P < 0.05). Similar data were obtained for IL-4 expression in both healthy individuals (<0.006) and asthmatic patients (<0.001). The increment of regulatory cytokines IL-10 and TGF-β expression was considerably increased in our investigation. Conclusion To our knowledge, this is the first report to document the suppressive effect that the M . marshalli ES product has on PBMSC cell culture of asthmatic patients. The present study provides new insights into understanding the immune modulation governed by parasite-derived products and the development of new asthma treatment strategies. [ABSTRACT FROM AUTHOR]