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链球菌坏死性软组织感染的发病机制。

Pathogenic Mechanisms of Streptococcal Necrotizing Soft Tissue Infections.

机构信息

Department of Molecular Genetics and Infection Biology, University of Greifswald, Greifswald, Germany.

Department of Medicine, Center for Infectious Medicine, Karolinska Institutet, Huddinge, Sweden.

出版信息

Adv Exp Med Biol. 2020;1294:127-150. doi: 10.1007/978-3-030-57616-5_9.

Abstract

Necrotizing skin and soft tissue infections (NSTIs) are severe life-threatening and rapidly progressing infections. Beta-hemolytic streptococci, particularly S. pyogenes (group A streptococci (GAS)) but also S. dysgalactiae subsp. equisimilis (SDSE, most group G and C streptococcus), are the main causative agents of monomicrobial NSTIs and certain types, such as emm1 and emm3, are over-represented in NSTI cases. An arsenal of bacterial virulence factors contribute to disease pathogenesis, which is a complex and multifactorial process. In this chapter, we summarize data that have provided mechanistic and immuno-pathologic insight into host-pathogens interactions that contribute to tissue pathology in streptococcal NSTIs. The role of streptococcal surface associated and secreted factors contributing to the hyper-inflammatory state and immune evasion, bacterial load in the tissue and persistence strategies, including intracellular survival and biofilm formation, as well as strategies to mimic NSTIs in vitro are discussed.

摘要

坏死性皮肤和软组织感染(NSTIs)是严重的危及生命的快速进展性感染。β-溶血性链球菌,特别是化脓性链球菌(A 组链球菌(GAS)),但也包括无乳链球菌亚群 equisimilis(SDSE,大多数 G 组和 C 组链球菌),是单一致病菌性 NSTIs 的主要病原体,某些类型,如 emm1 和 emm3,在 NSTI 病例中过度表达。细菌毒力因子的 arsenal 有助于疾病的发病机制,这是一个复杂的多因素过程。在本章中,我们总结了一些数据,这些数据为宿主-病原体相互作用提供了机制和免疫病理学见解,这些相互作用有助于链球菌 NSTIs 中的组织病理学。讨论了链球菌表面相关和分泌因子在超炎症状态和免疫逃逸中的作用、组织内细菌负荷和持久性策略,包括细胞内存活和生物膜形成,以及在体外模拟 NSTIs 的策略。

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