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血液和微囊泡的促凝活性受到肺炎球菌溶血素的干扰,后者与凝血因子相互作用。

Procoagulant Activity of Blood and Microvesicles Is Disturbed by Pneumococcal Pneumolysin, Which Interacts with Coagulation Factors.

机构信息

Institute of Medical Microbiology, Virology and Hygiene, Rostock University Medical Center, Rostock, Germany.

Department of Medicine, Clinic III-Hematology, Oncology, Palliative Medicine, Rostock University Medical Center, Rostock, Germany.

出版信息

J Innate Immun. 2023;15(1):136-152. doi: 10.1159/000525479. Epub 2022 Jul 15.

DOI:10.1159/000525479
PMID:35843205
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10643893/
Abstract

The coagulation and contact systems are parts of the innate immune system as they prevent bleeding and dissemination of pathogens and also contribute to microbial killing by inflammatory reactions and the release of antimicrobial peptides. Here, we investigated the influence of Streptococcus pneumoniae on the coagulation and contact system. S. pneumoniae (pneumococci), but no other investigated streptococcal species, impairs coagulation of blood by autolysis and release of pneumolysin. Defective blood coagulation results from the lysis of tissue factor-producing mononuclear cells and their procoagulant microvesicles, which are the main trigger for blood coagulation during sepsis. In addition, pneumolysin binds coagulation and contact system factors, but this does not result in activation. Thus, pneumococci modulate activation of the coagulation system by releasing pneumolysin, which could potentiate lung injury during pneumonia.

摘要

凝血和接触系统是先天免疫系统的一部分,因为它们可以防止出血和病原体的传播,还可以通过炎症反应和释放抗菌肽来帮助杀死微生物。在这里,我们研究了肺炎链球菌对凝血和接触系统的影响。肺炎链球菌(肺炎球菌),但其他研究的链球菌种没有,通过自溶和释放肺炎链球菌溶解素来损害血液的凝固。凝血功能障碍是由于产生组织因子的单核细胞及其促凝微囊泡的裂解引起的,这是脓毒症期间血液凝固的主要触发因素。此外,肺炎链球菌溶解素结合凝血和接触系统因子,但这不会导致激活。因此,肺炎链球菌通过释放肺炎链球菌溶解素来调节凝血系统的激活,这可能会在肺炎期间加重肺损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/99e6cceb63ef/jin-0015-0136-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/08a54a28ad09/jin-0015-0136-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/d9d1bcbc8305/jin-0015-0136-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/95f5b0b55649/jin-0015-0136-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/1c8592bff12c/jin-0015-0136-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/cbef3a5f5460/jin-0015-0136-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/3229ac9971af/jin-0015-0136-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/99e6cceb63ef/jin-0015-0136-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/08a54a28ad09/jin-0015-0136-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/d9d1bcbc8305/jin-0015-0136-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/95f5b0b55649/jin-0015-0136-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/1c8592bff12c/jin-0015-0136-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/cbef3a5f5460/jin-0015-0136-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/3229ac9971af/jin-0015-0136-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7284/10643893/99e6cceb63ef/jin-0015-0136-g07.jpg

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