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致病性协同作用:腹腔内混合感染

Pathogenic synergy: mixed intra-abdominal infections.

作者信息

MacLaren D M, Namavar F, Verweij-Van Vught A M, Vel W A, Kaan J A

出版信息

Antonie Van Leeuwenhoek. 1984;50(5-6):775-87. doi: 10.1007/BF02386240.

Abstract

In this article we review our researches into the pathogenesis of mixed infections. These may conveniently be divided into in vitro and in vivo studies. In vitro we confirmed that interference with the killing of aerobes by polymorphonuclear leucocytes (PMN's) is a property of the Bacteroides strains tested and appears to depend on competition for opsonins i.e. complement factors. Further studies are in progress to define which complement factors and which bacterial structures are involved. The influence of B. fragilis on chemotaxis has also been studied. Our preliminary data suggest that B. fragilis is itself poorly chemotactic and reduces the chemoattractivity of Proteus mirabilis. This observation is surprising when we consider that abscess formation is the hall-mark of B. fragilis infections and needs clarification. In vivo we have developed a skin infection model in mice which is economical and gives reproducible and quantitative results. In this model we have demonstrated pathogenic synergy between Escherichia coli and B. fragilis. Further studies are planned to assess the role of complement and bacterial factors in this in vivo synergy.

摘要

在本文中,我们回顾了对混合感染发病机制的研究。这些研究可方便地分为体外研究和体内研究。在体外,我们证实,多形核白细胞(PMN)对需氧菌杀灭作用的干扰是所测试拟杆菌菌株的一种特性,且似乎取决于对调理素即补体因子的竞争。进一步的研究正在进行,以确定涉及哪些补体因子和哪些细菌结构。脆弱拟杆菌对趋化性的影响也已得到研究。我们的初步数据表明,脆弱拟杆菌本身趋化性较差,并会降低奇异变形杆菌的化学吸引力。考虑到脓肿形成是脆弱拟杆菌感染的标志,这一观察结果令人惊讶,需要加以阐明。在体内,我们在小鼠中建立了一种皮肤感染模型,该模型经济实惠,能给出可重复的定量结果。在这个模型中,我们证明了大肠杆菌和脆弱拟杆菌之间的致病协同作用。计划进一步开展研究,以评估补体和细菌因子在这种体内协同作用中的作用。

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