Evaluation of Enterovirus infection in people with type 1 diabetes in Chaharmahal and Bakhtiari province compared to healthy subjects

زمینه و هدف: دیابت نوع 1، یک بیماری خود ایمنی چندعاملی بوده که برهمکنش عوامل ژنتیکی و محیطی می‌تواند سبب بروز آن شود. ویروس‌ها، ازجمله انتروویروس ها، از مهم‌ترین عوامل محیطی در پاتوژنز دیابت نوع 1 هستند. به‌منظور تعیین ارتباط میان انتروویروس ها و دیابت نوع 1 در جمعیت بیماران ایرانی، به بررسی میزان عفونت انتروویروسی در سرم بیماران مبتلا به دیابت نوع 1 پرداخته شد. روش بررسی: در این مطالعه‌ی مورد- شاهدی، برای تشخیص وجود RNA انتروویروسی، از تست Nested-PCR و برای تعیین کلاس‌های مختلف از آنتی بادی‌های ضد انتروویروسی نیز از تست الایزا استفاده شد. آزمون‌های آماری مورد استفاده در این مطالعه شامل آزمون دقیق فیشر و کای اسکوئر بود. یافته ها: از 35 نمونه سرمی جمع‌آوری‌شده از بیماران مبتلا به دیابت نوع 1، در سرم 12 بیمار (2/34) عفونت انتروویروسی به روش Nested-PCR مثبت شد، درحالی‌که تنها در یک مورد از افراد سالم مثبت بود (8/2) که اختلاف معنی داری را میان دو گروه نشان می دهد (05/0P<). آنتی‌بادی IgG ضد انتروویروسی در سرم 13 بیمار (1/37) و این آنتی‌بادی از کلاس IgA، در سرم 10 بیمار (5/28) یافت شد. این میزان در افراد سالم به ترتیب 3 (5/8) و 2 (7/5) نفر بود (برای هر دو آنتی بادی 05/0P<). آنتی بادی ضد انتروویروسی از کلاس IgM، در سرم هیچ‌یک از بیماران و افراد کنترل یافت نشد (1=P). نتیجه گیری: نتایج بدست آمده از این مطالعه نشان می‌دهد میزان شیوع عفونت انتروویروسی بیماران ایرانی مبتلا به دیابت نوع 1 به شکل معنی‌داری بالاتر از افراد سالم است. این مطالعه نوعی ارتباط میان انتروویروس ها و بیماری دیابت نوع 1 را در جمعیت مورد مطالعه نشان می‌دهد

Alteration in CD8+T cell subsets in enterovirus-infected patients: An alarming factor for type 1 diabetes mellitus

Type 1 diabetes is a multi-factorial disease that can develop due to the combination of genetic and environmental factors. Viruses, particularly enteroviruses, are major environmental candidates in the pathogenesis of type 1 diabetes, even though the mechanisms of pathogenicity of these viruses and their effects on the immune system have not been understood very well yet. Previous studies show that any imbalance in the population of different lymphocyte subsets could develop autoimmune diseases. Our theory is that enteroviral infection causes an impairment in the distribution of lymphocyte subtypes and consequently results in the diabetes onset in some individuals. Therefore, in this project, we evaluated the distribution of T CD8+ lymphocytes and their subsets in type 1 diabetes patients. This study was conducted to investigate the relationship between enteroviral infection and type 1 diabetes mellitus in an Iranian population, and suggestion a predicting approach for susceptible subjects. © 201

Alteration in CD8+ T cell subsets in enterovirus-infected patients: An alarming factor for type 1 diabetes mellitus

Type 1 diabetes is a multi-factorial disease that can develop due to the combination of genetic and environmental factors. Viruses, particularly enteroviruses, are major environmental candidates in the pathogenesis of type 1 diabetes, even though the mechanisms of pathogenicity of these viruses and their effects on the immune system have not been understood very well yet. Previous studies show that any imbalance in the population of different lymphocyte subsets could develop autoimmune diseases. Our theory is that enteroviral infection causes an impairment in the distribution of lymphocyte subtypes and consequently results in the diabetes onset in some individuals. Therefore, in this project, we evaluated the distribution of T CD8+ lymphocytes and their subsets in type 1 diabetes patients. This study was conducted to investigate the relationship between enteroviral infection and type 1 diabetes mellitus in an Iranian population, and suggestion a predicting approach for susceptible subjects

Alteration in CD8(+) T cell subsets in enterovirus-infected patients: An alarming factor for type 1 diabetes mellitus

Abstract Type 1 diabetes is a multi-factorial disease that can develop due to the combination of genetic and environmental factors. Viruses, particularly enteroviruses, are major environmental candidates in the pathogenesis of type 1 diabetes, even though the mechanisms of pathogenicity of these viruses and their effects on the immune system have not been understood very well yet. Previous studies show that any imbalance in the population of different lymphocyte subsets could develop autoimmune diseases. Our theory is that enteroviral infection causes an impairment in the distribution of lymphocyte subtypes and consequently results in the diabetes onset in some individuals. Therefore, in this project, we evaluated the distribution of T CD8+ lymphocytes and their subsets in type 1 diabetes patients. This study was conducted to investigate the relationship between enteroviral infection and type 1 diabetes mellitus in an Iranian population, and suggestion a predicting approach for susceptible subjects. Copyright (C) 2018, Kaohsiung Medical University. Published by Elsevier Taiwan LLC

Local Expression of Mucosal YKL-40; Correlation of YKL-40 with Clinical Manifestations and Immunopathogenesis of Moderate/Severe Persistent Allergic Rhinitis Patients

YKL-40 is an important protein that plays a critical role in chronic inflammation in hypersensitivity disease. In this study, the expression of YKL-40 was investigated among patients with moderate/severe persistent allergic rhinitis (M/S PAR), patients with mild (M) PAR and healthy individuals. Moreover, the association between YKL-40 and immunopathogenesis of M/S PAR was meticulously surveyed. For this purpose, surgical samples were tested by real-time polymerase chain reaction to evaluate YKL-40 mRNA expression. The presence and location of YKL-40 protein in the tissue samples were determined by immunohistochemistry. Additionally, we measured the number of eosinophils per field in the tissue samples, blood eosinophils, total serum IgE, specific serum IgE, total nasal syndrome score (TNSS) and YKL-40 serum levels. The data indicated that production of YKL-40 in patients with M/S PAR increased significantly when compared with the control group. Furthermore, local production of YKL-40 correlated with specific IgE, nasal eosinophil count and TNSS. The results of the present study indicate that YKL-40, for its correlation with allergic clinical manifestations and symptom severity in M/S PAR patients, should be considered as a trigger factor in AR

The relationship between IL-17A and IL-22 expression and clinical severity in patients with moderate/severe persistent allergic rhinitis

Purpose: Several reactions leading to numerous effects are regulated by IL-22. However, the relationship between IL-22 and immunopathogensis of allergic rhinitis (AR) has been rarely investigated. The aim of the present study was to investigate the levels of IL-22 and IL-17A in AR patients and their association with clinical severity of persistent allergic rhinitis (PAR). Materials and methods: Thirty mild persistent allergic rhinitis (M PAR) patients, thirty moderate/severe persistent allergic rhinitis (M/S PAR) patients, and thirty healthy controls were enrolled in this study. Local production of IL-22 and IL-17A in PAR patients and healthy controls' nasal mucosa was examined by immunohistochemistry (IHC) and real-time polymerase chain reaction (RT-PCR) techniques. Serum levels of IL-22, IL-17A, specific immunoglobulin E (sIgE), and total IgE (tIgE) in PAR patients and healthy controls were determined by ELISA. In addition, blood eosinophil, nasal eosinophils per field, and total nasal syndrome score (TNSS) were also assessed. Results: In comparison with healthy controls, production of IL-22 and IL-17A in M/S PAR patients increased significantly. Furthermore, serum levels as well as the mean number of IL-22 + and IL-17A + cells in nasal mucosa correlated with sIgE, nasal eosinophil count, and TNSS. Conclusion: The results of the present study provide the first evidence that local production of IL-22 might be expressed in PAR patients. The expression of IL-22 and IL-17A, and their correlations with clinical parameters in PAR patients suggest the role of these cytokines in the events involved in the development of PAR