دورية أكاديمية

Cholinergic anti-inflammatory pathway in the non-obese diabetic mouse model.

التفاصيل البيبلوغرافية
العنوان: Cholinergic anti-inflammatory pathway in the non-obese diabetic mouse model.
المؤلفون: Koopman, FA, Vosters, JL, Roescher, N, Broekstra, N, Tak, PP, Vervoordeldonk, MJ
المصدر: Oral Diseases; Oct2015, Vol. 21 Issue 7, p858-865, 8p, 1 Chart, 3 Graphs
مصطلحات موضوعية: ANALYSIS of variance, ANIMAL experimentation, BIOLOGICAL models, DIABETES, IMMUNOHISTOCHEMISTRY, INFLAMMATION, TYPE 1 diabetes, MICE, PARASYMPATHOMIMETIC agents, RESEARCH funding, SJOGREN'S syndrome, T-test (Statistics), DESCRIPTIVE statistics, KAPLAN-Meier estimator, LOG-rank test, MANN Whitney U Test, KRUSKAL-Wallis Test
مستخلص: Objective Activation of the cholinergic anti-inflammatory pathway ( CAP) has been shown to reduce inflammation in animal models, while abrogation of the pathway increases inflammation. We investigated whether modulation of CAP influences inflammation in the non-obese diabetic ( NOD) mouse model for Sjögren's syndrome and type 1 diabetes. Methods The alpha-7 nicotinic acetylcholine receptor ( α7n AChR) was stimulated with AR-R17779 or nicotine in NOD mice. In a second study, unilateral cervical vagotomy was performed. α7n AChR expression, focus scores, and salivary flow were evaluated in salivary glands ( SG) and insulitis score in the pancreas. Cytokines were measured in serum and SG. Results α7n AChR was expressed on myoepithelial cells in SG. Monocyte chemotactic protein-1 levels were reduced in SG after AR-R17779 treatment and tumor necrosis factor production was increased in the SG of the vagotomy group compared to controls. Focus score and salivary flow were unaffected. NOD mice developed diabetes more rapidly after vagotomy, but at completion of the study there were no statistically significant differences in number of mice that developed diabetes or in insulitis scores. Conclusion Intervention of the CAP in NOD mice leads to minimal changes in inflammatory cytokines, but did not affect overall inflammation and function of SG or development of diabetes. [ABSTRACT FROM AUTHOR]
Copyright of Oral Diseases is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
قاعدة البيانات: Complementary Index
الوصف
تدمد:1354523X
DOI:10.1111/odi.12354