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在革兰氏阴性菌肺炎所致脓毒症期间，造血细胞而非内皮细胞的髓样分化因子88（MyD88）有助于宿主防御。

Hematopoietic but not endothelial cell MyD88 contributes to host defense during gram-negative pneumonia derived sepsis.

作者信息

van Lieshout Miriam H P, Anas Adam A, Florquin Sandrine, Hou Baidong, van't Veer Cornelis, de Vos Alex F, van der Poll Tom

机构信息

Center of Infection and Immunity Amsterdam, Academic Medical Center, Amsterdam, The Netherlands; Center of Experimental and Molecular Medicine, Academic Medical Center, Amsterdam, the Netherlands.

Department of Pathology, Academic Medical Center, Amsterdam, the Netherlands.

出版信息

PLoS Pathog. 2014 Sep 25;10(9):e1004368. doi: 10.1371/journal.ppat.1004368. eCollection 2014 Sep.

DOI:10.1371/journal.ppat.1004368
PMID:25254554
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4177915/
Abstract

Klebsiella pneumoniae is an important cause of sepsis. The common Toll-like receptor adapter myeloid differentiation primary response gene (MyD)88 is crucial for host defense against Klebsiella. Here we investigated the role of MyD88 in myeloid and endothelial cells during Klebsiella pneumosepsis. Mice deficient for MyD88 in myeloid (LysM-Myd88(-/-)) and myeloid plus endothelial (Tie2-Myd88(-/-)) cells showed enhanced lethality and bacterial growth. Tie2-Myd88(-/-) mice reconstituted with control bone marrow, representing mice with a selective MyD88 deficiency in endothelial cells, showed an unremarkable antibacterial defense. Myeloid or endothelial cell MyD88 deficiency did not impact on lung pathology or distant organ injury during late stage sepsis, while LysM-Myd88(-/-) mice demonstrated a strongly attenuated inflammatory response in the airways early after infection. These data suggest that myeloid but not endothelial MyD88 is important for host defense during gram-negative pneumonia derived sepsis.

摘要

肺炎克雷伯菌是脓毒症的一个重要病因。常见的Toll样受体衔接蛋白髓样分化初级反应基因（MyD）88对于宿主抵御克雷伯菌至关重要。在此，我们研究了MyD88在肺炎克雷伯菌脓毒症期间髓样细胞和内皮细胞中的作用。髓样细胞（LysM-Myd88(-/-)）以及髓样细胞加内皮细胞（Tie2-Myd88(-/-)）中缺乏MyD88的小鼠表现出更高的致死率和细菌生长。用对照骨髓重建的Tie2-Myd88(-/-)小鼠，代表在内皮细胞中存在选择性MyD88缺陷的小鼠，其抗菌防御并无异常。在晚期脓毒症期间，髓样或内皮细胞MyD88缺陷对肺部病理或远处器官损伤并无影响，而LysM-Myd88(-/-)小鼠在感染后早期气道中的炎症反应明显减弱。这些数据表明，在革兰氏阴性菌肺炎所致脓毒症期间，髓样细胞而非内皮细胞中的MyD88对宿主防御至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df83/4177915/ce1cc0151a2e/ppat.1004368.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df83/4177915/3350bdd80763/ppat.1004368.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df83/4177915/d82056cbf72c/ppat.1004368.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df83/4177915/4e0b02574338/ppat.1004368.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df83/4177915/5e6e32a1caab/ppat.1004368.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df83/4177915/2f02a7b307ec/ppat.1004368.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df83/4177915/ce1cc0151a2e/ppat.1004368.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df83/4177915/3350bdd80763/ppat.1004368.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df83/4177915/d82056cbf72c/ppat.1004368.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df83/4177915/4e0b02574338/ppat.1004368.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df83/4177915/5e6e32a1caab/ppat.1004368.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df83/4177915/2f02a7b307ec/ppat.1004368.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df83/4177915/ce1cc0151a2e/ppat.1004368.g006.jpg

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