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蜜蜂感染幼虫芽孢杆菌(美洲幼虫腐臭病的病原体)期间,蜜蜂幼虫围食膜的降解是发病机制中的关键步骤。

Honey bee larval peritrophic matrix degradation during infection with Paenibacillus larvae, the aetiological agent of American foulbrood of honey bees, is a key step in pathogenesis.

作者信息

Garcia-Gonzalez Eva, Genersch Elke

机构信息

Department for Molecular Microbiology and Bee Diseases, Institute for Bee Research, Friedrich-Engels-Str 32, 16540 Hohen Neuendorf, Germany.

Humboldt Universität Berlin, Institut für Biologie, Bakteriengenetik, Chausseestrasse 117, 10115, Berlin, Germany.

出版信息

Environ Microbiol. 2013 Nov;15(11):2894-901. doi: 10.1111/1462-2920.12167. Epub 2013 Jun 27.

DOI:10.1111/1462-2920.12167
PMID:23809335
Abstract

Paenibacillus larvae, the aetiological agent of American foulbrood (AFB) of honey bees, causes a fatal intestinal infection in larvae and invades the haemocoel by breaching the midgut. The peritrophic matrix lining the midgut epithelium in insects constitutes an effective barrier against abrasive food particles, xenobiotics, toxins and pathogens. Pathogens like P. larvae entering the host through the gut first need to overcome this barrier. To better understand AFB pathogenesis, we analysed the fate of the peritrophic matrix in honey bee larvae during P. larvae infection. Using histochemical techniques, we first established that chitin is a major component of the honey bee larval peritrophic matrix. Rearing larvae on a diet containing a fluorochrome blocking formation of the peritrophic matrix or a bacterial endochitinase revealed that a fully formed peritrophic matrix is essential for larval survival. Larvae infected by P. larvae showed total degradation of the peritrophic matrix enabling the bacteria to directly attack the epithelial cells. Carbon source utilization tests confirmed that P. larvae is able to metabolize colloidal chitin. We propose that P. larvae degrades the peritrophic matrix to allow direct access of the bacteria or of bacterial toxins to the epithelium to prepare the breakthrough of the epithelial layer.

摘要

幼虫芽孢杆菌是蜜蜂美洲幼虫腐臭病(AFB)的病原体,可在幼虫中引起致命的肠道感染,并通过突破中肠侵入血腔。昆虫中肠上皮内衬的围食膜构成了一道有效的屏障,可抵御粗糙的食物颗粒、异生物素、毒素和病原体。像幼虫芽孢杆菌这样通过肠道进入宿主的病原体首先需要克服这道屏障。为了更好地理解AFB的发病机制,我们分析了幼虫芽孢杆菌感染期间蜜蜂幼虫围食膜的命运。我们首先使用组织化学技术确定几丁质是蜜蜂幼虫围食膜的主要成分。在含有阻止围食膜形成的荧光染料或细菌内切几丁质酶的饮食中饲养幼虫,结果表明完全形成的围食膜对幼虫存活至关重要。受幼虫芽孢杆菌感染的幼虫显示围食膜完全降解,使细菌能够直接攻击上皮细胞。碳源利用测试证实幼虫芽孢杆菌能够代谢胶体几丁质。我们提出,幼虫芽孢杆菌降解围食膜,使细菌或细菌毒素能够直接接触上皮,为突破上皮层做好准备。

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