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琥珀酸是拟杆菌属的一种代谢副产物,可抑制多形核白细胞的功能。

Succinic acid, a metabolic by-product of Bacteroides species, inhibits polymorphonuclear leukocyte function.

作者信息

Rotstein O D, Pruett T L, Fiegel V D, Nelson R D, Simmons R L

出版信息

Infect Immun. 1985 May;48(2):402-8. doi: 10.1128/iai.48.2.402-408.1985.

DOI:10.1128/iai.48.2.402-408.1985
PMID:3886546
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC261327/
Abstract

Anaerobes, in particular Bacteroides spp., are the predominant bacteria present in mixed intra-abdominal infections, yet their critical importance in the pathogenicity of these infections is not clearly defined. Succinic acid, a major fatty acid by-product of Bacteroides metabolism, was tested for its effect on neutrophil function to determine whether it might play a role in enhancing the virulence of Bacteroides-containing infections. At pH 5.5 but not pH 7.0, succinic acid at concentrations commonly found in clinical abscesses profoundly inhibits in vitro neutrophil function. It virtually obliterates phagocytic killing of Escherichia coli and reduces neutrophil random migration and chemotactic response to formyl-methionyl-leucyl-phenylalanine and C5a. These effects occur in conjunction with a reduced chemiluminescent peak and delayed time to the peak. The effect on neutrophils is only partially reversible by multiple washings. These findings suggest that succinic acid may be an important Bacteroides virulence factor when present in the microenvironment of a mixed intra-abdominal infection in which concentrations are high and the pH of the medium is reduced.

摘要

厌氧菌,尤其是拟杆菌属,是腹腔内混合感染中存在的主要细菌,然而它们在这些感染的致病性中的关键重要性尚未明确界定。琥珀酸是拟杆菌代谢的主要脂肪酸副产物,测试了其对中性粒细胞功能的影响,以确定它是否可能在增强含拟杆菌感染的毒力中发挥作用。在pH 5.5而非pH 7.0时,临床脓肿中常见浓度的琥珀酸会显著抑制体外中性粒细胞功能。它几乎消除了对大肠杆菌的吞噬杀伤作用,并减少了中性粒细胞的随机迁移以及对甲酰甲硫氨酰亮氨酰苯丙氨酸和C5a的趋化反应。这些效应伴随着化学发光峰值降低和达到峰值的时间延迟。多次洗涤只能部分逆转对中性粒细胞的影响。这些发现表明,当琥珀酸存在于腹腔内混合感染的微环境中,浓度较高且培养基pH降低时,它可能是拟杆菌的一种重要毒力因子。

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Succinic acid, a metabolic by-product of Bacteroides species, inhibits polymorphonuclear leukocyte function.琥珀酸是拟杆菌属的一种代谢副产物,可抑制多形核白细胞的功能。
Infect Immun. 1985 May;48(2):402-8. doi: 10.1128/iai.48.2.402-408.1985.
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