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病原体毒力通过抑制蛋白质消化阻碍共生介导的宿主幼体生长增强。

Pathogen Virulence Impedes Mutualist-Mediated Enhancement of Host Juvenile Growth via Inhibition of Protein Digestion.

作者信息

Erkosar Berra, Storelli Gilles, Mitchell Mélanie, Bozonnet Loan, Bozonnet Noémie, Leulier François

机构信息

Institut de Génomique Fonctionnelle de Lyon, Ecole Normale Supérieure de Lyon, Centre National de la Recherche Scientifique, Université Claude Bernard Lyon 1, Unité Mixte de Recherche 5242, 69364 Lyon, Cedex 07, France.

Institut de Génomique Fonctionnelle de Lyon, Ecole Normale Supérieure de Lyon, Centre National de la Recherche Scientifique, Université Claude Bernard Lyon 1, Unité Mixte de Recherche 5242, 69364 Lyon, Cedex 07, France.

出版信息

Cell Host Microbe. 2015 Oct 14;18(4):445-55. doi: 10.1016/j.chom.2015.09.001. Epub 2015 Oct 1.

DOI:10.1016/j.chom.2015.09.001
PMID:26439865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4617634/
Abstract

The microbial environment impacts many aspects of metazoan physiology through largely undefined molecular mechanisms. The commensal strain Lactobacillus plantarum(WJL) (Lp(WJL)) sustains Drosophila hormonal signals that coordinate systemic growth and maturation of the fly. Here we examine the underlying mechanisms driving these processes and show that Lp(WJL) promotes intestinal peptidase expression, leading to increased intestinal proteolytic activity, enhanced dietary protein digestion, and increased host amino acid levels. Lp(WJL)-mediated peptidase upregulation is partly driven by the peptidoglycan recognition and signaling cascade PGRP-LE/Imd/Relish. Additionally, this mutualist-mediated physiological benefit is antagonized upon pathogen infection. Pathogen virulence selectively impedes Lp(WJL)-mediated intestinal peptidase activity enhancement and juvenile growth promotion but does not alter growth of germ-free animals. Our study reveals the adaptability of host physiology to the microbial environment, whereby upon acute infection the host switches to pathogen-mediated host immune defense at the expense of mutualist-mediated growth promotion.

摘要

微生物环境通过很大程度上未知的分子机制影响后生动物生理学的许多方面。共生菌株植物乳杆菌（WJL）（Lp（WJL））维持果蝇的激素信号，这些信号协调果蝇的全身生长和成熟。在这里，我们研究驱动这些过程的潜在机制，并表明Lp（WJL）促进肠道肽酶表达，导致肠道蛋白水解活性增加、膳食蛋白质消化增强和宿主氨基酸水平升高。Lp（WJL）介导的肽酶上调部分由肽聚糖识别和信号级联PGRP-LE/Imd/Relish驱动。此外，这种共生体介导的生理益处会在病原体感染时受到拮抗。病原体毒力选择性地阻碍Lp（WJL）介导的肠道肽酶活性增强和幼虫生长促进，但不会改变无菌动物的生长。我们的研究揭示了宿主生理学对微生物环境的适应性，即在急性感染时，宿主会转向病原体介导的宿主免疫防御，以牺牲共生体介导的生长促进为代价。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/b35cc2a30e78/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/456eaad7a247/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/09faf4cfe4e2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/1adad8926875/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/1c5f44d84d4a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/d123215550c8/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/27ac7883a3ff/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/22bf57d9a11f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/b35cc2a30e78/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/456eaad7a247/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/09faf4cfe4e2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/1adad8926875/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/1c5f44d84d4a/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/d123215550c8/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/27ac7883a3ff/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/22bf57d9a11f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2b17/4617634/b35cc2a30e78/gr7.jpg

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