کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10172105 | 1225758 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Viral infections in asthma and COPD
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کلمات کلیدی
AHRIPS-1D-GalNPI3KδMDA5RIG-IRSVTLR3PD-1Nrf2d-Galactosamine - d-گالاکتوزامینHRV - ENGTRIF - Trif بهAsthma - آسمinflammation - التهاب( توروم) Innate immunity - ایمنی ذاتیCOPD - بیماری مزمن انسدادی ریهHuman rhinovirus - رینوویروس انسانیLAI - شبیهLower airway infection - عفونت دستگاه تنفسی پایینProgrammed death-1 - مرگ برنامه ریزی شده 1Virus - ویروسRespiratory syncytial virus - ویروس سنسیتیال تنفسیAirway hyperresponsiveness - پاسخگویی فوریPoly IC - پلی ICpolyinosinic-polycytidylic acid - پلیسی سمی-پلیسییدیدیل اسیدmelanoma differentiation-associated gene 5 - ژن 5 مرتبط با تمایز ملانوم 5retinoic acid-inducible gene I - ژن I القاء شده اسید رتینوئیکToll-like receptor 3 - گیرنده پولی 3
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی و میکروب شناسی (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Viral infections in asthma and COPD Viral infections in asthma and COPD](/preview/png/10172105.png)
چکیده انگلیسی
Airway viral infections are associated with the pathogenesis of asthma and COPD. It has been argued that respiratory syncytial virus (RSV) infection in infancy is a probable causal factor in the development of pediatric asthma. RSV infections tend to induce Th2-biased immune responses in the host airways. RSV infection, atopy, and low pulmonary function in neonates may work synergistically toward the development of pediatric asthma. Human rhinovirus (HRV) is a representative virus associated with the exacerbation of asthma in both children and adults. Viral infections trigger innate immune responses including granulocytic inflammation and worsen the underlying inflammation due to asthma and COPD. The innate immune responses involve type-I and -III interferon (IFN) production, which plays an important role in anti-viral responses, and the airway epithelia of asthmatics reportedly exhibit defects in the virus-induced IFN responses, which renders these individuals more susceptible to viral infection. A similarly impaired IFN response is seen in COPD, and several investigators propose that latent adenoviral infection may be involved in COPD development. Persistent RSV infections were detected in a sub-population of patients with COPD and were associated with the accelerated decline of lung function. The virus-induced upregulation of co-inhibitory molecules in the airway epithelium partly accounts for the persistent infections. Experimental animal models for virus-asthma/COPD interactions have shed light on the underlying immune mechanisms and are expected to help develop novel approaches to treat respiratory diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Respiratory Investigation - Volume 52, Issue 2, March 2014, Pages 92-100
Journal: Respiratory Investigation - Volume 52, Issue 2, March 2014, Pages 92-100
نویسندگان
Koichiro Matsumoto, Hiromasa Inoue,