ABSTRACT
BACKGROUND: Rotavirus (RV) has been postulated as a viral trigger for the onset of autoimmune disorders, such as type 1 diabetes (T1D). This study aimed to examine the conceivable association of RV IgG with cytokine levels and dyslipidemia in the pathogenesis of pediatric T1D. METHODS: This study included 30 healthy controls and 80 children with T1D who were divided into two groups based on the time since their T1D diagnosis: newly diagnosed (ND ≤ 1 year; n = 30) and previously diagnosed (PD > 1 year; n = 50). ND and PD patients were also separated into negative and positive according to IgG detection (RV IgG-, ND-, and PD-; RV IgG+, ND+, and PD+). RESULTS: Positive polymerase chain reaction for RVs was evidenced in 7.5% of children with T1D. Anti-RV IgG was 30% and 36% in ND and PD, respectively, compared to healthy controls (2 of 30, 6.6%; P < 0.05). Fasting blood sugar and hemoglobin A1c significantly increased in PD+ compared to PD-. Interferon-γ and interleukin (IL)-15 levels significantly increased. IL-12 and IL-22 mRNA expression was upregulated in ND+ patients compared to that in ND- patients. IL-37 mRNA expression was significantly downregulated in ND- and ND+ patients compared to that in healthy controls. Total cholesterol and high- and low-density lipoprotein-cholesterol levels were significantly lower in PD+ than in PD-; whereas triglyceride levels were higher than those in healthy controls. CONCLUSIONS: This study suggested that anti-RV IgG may have a role in the pathogenesis, development, and progression of T1D, and RV infections are implicated in dyslipidemia and inflammation status.
Subject(s)
Diabetes Mellitus, Type 1 , Dyslipidemias , Rotavirus , Antibodies, Viral , Child , Cholesterol , Cytokines/genetics , Cytokines/metabolism , Diabetes Mellitus, Type 1/complications , Diabetes Mellitus, Type 1/genetics , Dyslipidemias/complications , Dyslipidemias/genetics , Humans , Immunoglobulin G , RNA, Messenger , Rotavirus/genetics , Rotavirus/metabolismABSTRACT
Virological responses after hepatitis C virus (HCV) treatment may alleviate liver disease and extra-hepatic manifestations. Our study aims to explore the impact of HCV eradication on the glycemic status, insulin resistance, cytokine production, and insulin receptor substrate (IRS)-1 and 2 gene expression levels in HCV-hyperglycemic patients. A total of 90 participants were allocated as follows: Group 1 included 30 healthy subjects as controls, and Group 2 included 60 HCV-hyperglycemic patients treated with a direct-acting antiviral (DAA) regimen and further subdivided into HCV-pre-diabetic and HCV-diabetic groups. Laboratory assays screened patients before and after treatments. Our data showed an excellent rate of virological responses in HCV groups after HCV treatment. Moreover, HCV eradication significantly ameliorated blood glucose levels and insulin resistance biomarkers in HCV-hyperglycemic patients compared with baseline values. Also, interleukin (IL)-6, IL-17, IL-23, and IL-27 levels were significantly ameliorated after viral clearance in HCV-hyperglycemic patients compared with baseline values. Similarly, IRS-1 and 2 mRNA expression levels were upregulated in these patients post-HCV treatment compared with baseline values. HCV clearance ameliorated hyperglycemia, cytokine production, and enhanced insulin sensitivity. Future researches will be needed to explore the effects of cytokines and IRS on HCV infection and treatment on a large cohort.
Subject(s)
Hepatitis C, Chronic , Hepatitis C , Hyperglycemia , Insulin Resistance , Interleukin-27 , Humans , Hepacivirus , Insulin Resistance/physiology , Antiviral Agents/therapeutic use , Insulin Receptor Substrate Proteins/genetics , Insulin Receptor Substrate Proteins/metabolism , Interleukin-17 , Hepatitis C, Chronic/drug therapy , Blood Glucose , Receptor, Insulin/metabolism , Receptor, Insulin/pharmacology , Receptor, Insulin/therapeutic use , Interleukin-27/metabolism , Interleukin-27/pharmacology , Interleukin-27/therapeutic use , Hepatitis C/complications , Hepatitis C/drug therapy , Hyperglycemia/drug therapy , Gene Expression , Interleukin-23 , RNA, MessengerABSTRACT
BACKGROUND AND OBJECTIVES: The fibrosing forms of interstitial lung disease (ILD) are associated with significant morbidity and mortality. ILD may be idiopathic, secondary to occupational, infection, complicate rheumatic diseases or drug induced. Efficacy of antifibrotic agents is as far as, limited and uncertain. No effective treatment was confirmed for pulmonary fibrosis except lung transplantation. The present study aimed at investigating the possible effect of human cord blood mesenchymal stem cell (MSC) therapy on fibrosing ILD. This was accomplished by using amiodarone as a model of induced lung damage in albino rat. METHODS AND RESULTS: Seventeen adult male albino rats were divided into 3 groups. Rats of amiodarone group were given 30 mg/kg of amiodarone orally 6 days/ week for 6 weeks. Rats of stem cell therapy group were injected with stem cells in the tail vein following confirmation of lung damage and left for 4 weeks before sacrifice. Obstructed bronchioles, thickened interalveolar septa and thickened wall of pulmonary vessels were found and proved morphometrically. Reduced type I pneumocytes and increased area% of collagen fibers were recorded. All findings regressed on stem cell therapy. CONCLUSIONS: Cord blood MSC therapy proved definite amelioration of fibrosing interstitial lung disease provided therapy starts early in the development of the pathogenesis.
