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本文引用的文献

1
Higher titers of anti-Chlamydia pneumoniae IgG in diabetic retinopathy: a cross-sectional study.糖尿病视网膜病变患者血清抗肺炎衣原体 IgG 抗体滴度升高:一项横断面研究。
Diabetes Metab Res Rev. 2015 Feb;31(2):168-74. doi: 10.1002/dmrr.2581. Epub 2014 Sep 14.
2
Hepatic overexpression of ATP synthase β subunit activates PI3K/Akt pathway to ameliorate hyperglycemia of diabetic mice.肝过度表达 ATP 合酶β亚基激活 PI3K/Akt 通路以改善糖尿病小鼠的高血糖症。
Diabetes. 2014 Mar;63(3):947-59. doi: 10.2337/db13-1096. Epub 2013 Dec 2.
3
Sociocultural and socioeconomic influences on type 2 diabetes risk in overweight/obese African-American and Latino-American children and adolescents.社会文化和社会经济因素对超重/肥胖非裔美国和拉丁裔美国儿童及青少年2型糖尿病风险的影响。
J Obes. 2013;2013:512914. doi: 10.1155/2013/512914. Epub 2013 May 13.
4
Activation of inflammasome signaling mediates pathology of acute P. aeruginosa pneumonia.炎症小体信号的激活介导了急性铜绿假单胞菌肺炎的病理学过程。
J Clin Invest. 2013 Apr;123(4):1630-7. doi: 10.1172/JCI66142. Epub 2013 Mar 8.
5
Mast cell TLR2 signaling is crucial for effective killing of Francisella tularensis.肥大细胞 TLR2 信号对于有效杀伤土拉弗朗西斯菌至关重要。
J Immunol. 2012 Jun 1;188(11):5604-11. doi: 10.4049/jimmunol.1200039. Epub 2012 Apr 23.
6
Prevalence of obesity and trends in the distribution of body mass index among US adults, 1999-2010.美国成年人肥胖率及体重指数分布的趋势:1999-2010 年。
JAMA. 2012 Feb 1;307(5):491-7. doi: 10.1001/jama.2012.39. Epub 2012 Jan 17.
7
The inflammasome: an integrated view.炎症小体:综合观点。
Immunol Rev. 2011 Sep;243(1):136-51. doi: 10.1111/j.1600-065X.2011.01046.x.
8
Increased TLR2 expression in patients with type 1 diabetes: evidenced risk of microalbuminuria.1 型糖尿病患者 TLR2 表达增加:微量白蛋白尿的风险证据。
Pediatr Diabetes. 2012 Mar;13(2):147-54. doi: 10.1111/j.1399-5448.2011.00794.x. Epub 2011 Aug 17.
9
Caspase-1 dependent IL-1β secretion is critical for host defense in a mouse model of Chlamydia pneumoniae lung infection.半胱天冬酶-1 依赖性白细胞介素-1β分泌对于肺炎衣原体肺部感染小鼠模型中的宿主防御至关重要。
PLoS One. 2011;6(6):e21477. doi: 10.1371/journal.pone.0021477. Epub 2011 Jun 23.
10
Type 2 diabetes as an inflammatory disease.2 型糖尿病作为一种炎症性疾病。
Nat Rev Immunol. 2011 Feb;11(2):98-107. doi: 10.1038/nri2925. Epub 2011 Jan 14.

肺炎衣原体促进胰腺β细胞功能障碍。

Chlamydia pneumoniae promotes dysfunction of pancreatic beta cells.

作者信息

Rodriguez Annette R, Plascencia-Villa Germán, Witt Colleen M, Yu Jieh-Juen, José-Yacamán Miguel, Chambers James P, Perry George, Guentzel M Neal, Arulanandam Bernard P

机构信息

RCMI Biophotonics Core, University of Texas at San Antonio, One UTSA Circle, San Antonio, TX 78249, United States.

RCMI Nanotechnology and Human Health Core, Department of Physics, University of Texas at San Antonio, One UTSA Circle, San Antonio, TX 78249, United States.

出版信息

Cell Immunol. 2015 Jun;295(2):83-91. doi: 10.1016/j.cellimm.2015.03.010. Epub 2015 Apr 1.

DOI:10.1016/j.cellimm.2015.03.010
PMID:25863744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4533996/
Abstract

The human pathogen Chlamydia pneumoniae has been implicated in chronic inflammatory diseases including type 2 diabetes. Therefore, we designed a study to evaluate pancreatic beta cells and mast cells during chlamydial infection. Our study revealed that C. pneumoniae infected mast cells significantly (p<0.005) decreased beta cell ATP and insulin production, in contrast to uninfected mast cells co-cultured with beta cells. Infected mast cells exhibited pyknotic nuclei and active caspase-3 and caspase-1 expression. Additionally, ex vivo analyses of tissues collected from C. pneumoniae infected mice showed increased interleukin-1β production in splenocytes and pancreatic tissues as was observed with in vitro mast cell-beta cell co-cultures during C. pneumoniae infection. Notably, infected mast cells promoted beta cell destruction. Our findings reveal the negative effect of C. pneumoniae on mast cells, and the consequential impact on pancreatic beta cell function and viability.

摘要

人类病原体肺炎衣原体与包括2型糖尿病在内的慢性炎症性疾病有关。因此,我们设计了一项研究来评估衣原体感染期间的胰腺β细胞和肥大细胞。我们的研究表明,与与β细胞共培养的未感染肥大细胞相比,肺炎衣原体感染的肥大细胞显著(p<0.005)降低了β细胞的三磷酸腺苷(ATP)和胰岛素生成。受感染的肥大细胞表现出核固缩以及活性半胱天冬酶-3和半胱天冬酶-1的表达。此外,对从肺炎衣原体感染小鼠收集的组织进行的体外分析显示,脾细胞和胰腺组织中白细胞介素-1β的生成增加,这与肺炎衣原体感染期间体外肥大细胞与β细胞共培养时观察到的情况一致。值得注意的是,受感染的肥大细胞促进了β细胞的破坏。我们的研究结果揭示了肺炎衣原体对肥大细胞产生的负面影响,以及对胰腺β细胞功能和活力的相应影响。