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啮齿动物局部和全身感染模型中脂肪组织的固有免疫

Innate Immunity of Adipose Tissue in Rodent Models of Local and Systemic Infection.

作者信息

Schmid Andreas, Karrasch Thomas, Thomalla Miriam, Schlegel Jutta, Salzberger Bernd, Schäffler Andreas, Hanses Frank

机构信息

Department of Internal Medicine III, Giessen University Hospital, 35392 Giessen, Germany.

Infectious Diseases Unit, Regensburg University Hospital, 93053 Regensburg, Germany.

出版信息

Mediators Inflamm. 2017;2017:5315602. doi: 10.1155/2017/5315602. Epub 2017 Mar 27.

DOI:10.1155/2017/5315602
PMID:28428684
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5385907/
Abstract

. The role of adipose tissue in systemic inflammation during bacterial infection is unclear. Effects of infection on adipocytes in rodent models of experimental endocarditis and peritonitis, the impact of infection on gene expression in epididymal and subcutaneous adipose tissue, and effects of infection on the toll-like receptor-2- (TLR2-) cathelicidin pathway in vivo and in vitro were investigated. The rat model of catheter-induced endocarditis and the mouse model of -induced peritonitis were used for infection experiments, gene expression profiling in adipose tissue, and measurement of cytokines. 3T3-L1 adipocytes were analyzed for expression of the TLR2-cathelicidin pathway. . Upon systemic bacterial infection by , there is a shift from anti- to proinflammatory cytokines in serum and in adipose tissue gene expression. The TLR2-cathelicidin pathway is increasingly expressed during adipocyte differentiation in vitro and is induced upon stimulation by synthetic lipopeptides. . Systemic infection by Gram-positive bacteria induces proinflammatory transformation of adipose tissue sites distinct from infection sites, documented on the levels of gene expression and secreted mediators. The TLR2-cathelicidine pathway is expressed and highly inducible in adipocytes in vitro. Lipopeptides are important immune-modulators of adipocytes in both gene expression and protein secretion.

摘要

脂肪组织在细菌感染期间全身炎症反应中的作用尚不清楚。研究了感染对实验性心内膜炎和腹膜炎啮齿动物模型中脂肪细胞的影响、感染对附睾和皮下脂肪组织基因表达的影响，以及感染对体内外Toll样受体2（TLR2）-杀菌肽途径的影响。采用导管诱导的心内膜炎大鼠模型和诱导性腹膜炎小鼠模型进行感染实验、脂肪组织基因表达谱分析及细胞因子检测。对3T3-L1脂肪细胞进行TLR2-杀菌肽途径表达分析。感染后，血清和脂肪组织基因表达中出现从抗炎细胞因子向促炎细胞因子的转变。TLR2-杀菌肽途径在体外脂肪细胞分化过程中表达增加，并在合成脂肽刺激后被诱导。革兰氏阳性菌的全身感染诱导了与感染部位不同的脂肪组织部位的促炎转变，这在基因表达水平和分泌介质中得到证实。TLR2-杀菌肽途径在体外脂肪细胞中表达且高度可诱导。脂肽在基因表达和蛋白质分泌方面都是脂肪细胞重要的免疫调节剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ee/5385907/5e9ae1f143ab/MI2017-5315602.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ee/5385907/66381f4c3bf1/MI2017-5315602.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ee/5385907/4f62d73e3966/MI2017-5315602.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ee/5385907/5e9ae1f143ab/MI2017-5315602.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ee/5385907/66381f4c3bf1/MI2017-5315602.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ee/5385907/4f62d73e3966/MI2017-5315602.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ee/5385907/5e9ae1f143ab/MI2017-5315602.003.jpg

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