Diabetes prolongs the inflammatory response to a bacterial stimulus through cytokine dysregulation
Diabetes prolongs the inflammatory response to a bacterial stimulus through cytokine dysregulation
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DOI：
10.1111/j.0022-202x.2004.22711.x
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发表时间：
2004-07-01
影响因子：
6.5
通讯作者：
Graves, DT
中科院分区：
文献类型：
--
作者：
Naguib, G;Al-Mashat, H;Graves, DT
糖尿病已被确定为感染的重要危险因素。但是，关于糖尿病如何改变对细菌的炎症反应，人们知之甚少。本研究的目的是通过关注结缔组织环境中的炎症反应来研究糖尿病如何影响宿主-细菌相互作用。糖尿病（db/db）和对照（db/+）小鼠接种牙龈卟啉单胞菌，一种与咬伤和牙周病相关的病原体。通过组织学或炎性细胞因子的表达来测量反应。通过定量组织学分析，在第1天糖尿病小鼠和对照小鼠之间几乎没有差异。然而，在第3天，对照组的炎症浸润已经消退，而糖尿病组则没有（p
Diabetes has been identified as an important risk factor for infection. But relatively little is known about how diabetes alters the inflammatory response to bacteria. The objective of this study was to investigate how diabetes affects host-bacteria interactions by focusing on the inflammatory response in a connective tissue setting. Diabetic (db/db) and control (db/+) mice were inoculated with Porphyromonas gingivalis, a pathogen associated with bite wounds and periodontal disease. The response was measured histologically or by the expression of inflammatory cytokines. By quantitative histologic analysis, there was little difference between the diabetic and control mice on day 1. On day 3, however, the inflammatory infiltrate had subsided in the control group, whereas it had not in the diabetic group (p