Immune dysfunction in patients with diabetes mellitus (DM)

Immune dysfunction in patients with diabetes mellitus (DM)
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DOI:
10.1016/s0928-8244(99)00142-x
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发表时间:
1999-12-01
影响因子:
--
通讯作者:
Hoepelman, AIM
Hoepelman, AIM
中科院分区:
其他
文献类型:
--
作者:
Geerlings, SE;Hoepelman, AIM

文献摘要

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糖尿病(DM)患者比非DM患者更常发生感染。在这一患者群体中,感染的过程也更复杂。感染率增加的可能原因之一是免疫缺陷。除了一些体外细胞反应降低外,没有描述糖尿病患者的适应性免疫紊乱。在糖尿病患者中已经描述了体液先天免疫中的不同紊乱(低补体因子4、刺激后细胞因子应答降低)。然而,这些发现的临床相关性尚不清楚。关于细胞先天免疫,大多数研究显示,与对照细胞相比,糖尿病多形核细胞和糖尿病单核细胞/巨噬细胞的功能(趋化性、吞噬作用、杀伤作用)降低。一般来说,DM的更好调节导致这些细胞功能的改善。此外,一些微生物在高葡萄糖环境中变得更具毒性。另一种可能导致糖尿病患者感染患病率增加的机制是与非糖尿病细胞相比,微生物对糖尿病细胞的粘附增加。这已被描述为白色念珠菌。可能受体的碳水化合物组成在这种现象中起作用。(C)1999年,欧洲微生物学会联合会。由Elsevier Science B. V.出版,版权所有。
Patients with diabetes mellitus (DM) have infections more often than those without DM. The course of the infections is also more complicated in this patient group. One of the possible causes of this increased prevalence of infections is defects in immunity. Besides some decreased cellular responses in vitro, no disturbances in adaptive immunity in diabetic patients have been described. Different disturbances (low complement factor 4, decreased cytokine response after stimulation) in humoral innate immunity have been described in diabetic patients. However, the clinical relevance of these findings is not clear. Concerning cellular innate immunity most studies show decreased functions (chemotaxis, phagocytosis, killing) of diabetic polymorphonuclear cells and diabetic monocytes/macrophages compared to cells of controls. In general, a better regulation of the DM leads to an improvement of these cellular functions. Furthermore, some microorganisms become more virulent in a high glucose environment. Another mechanism which can lead to the increased prevalence of infections in diabetic patients is an increased adherence of microorganisms to diabetic compared to nondiabetic cells. This has been described for Candida albicans. Possibly the carbohydrate composition of the receptor plays a role in this phenomenon. (C) 1999 Federation of European Microbiological Societies. Published by Elsevier Science B.V. All rights reserved.