Group A Streptococcus (GAS) has a fantastically wide tissue tropism in humans, manifesting as different diseases depending on the strain’s virulence factor repertoire and the tissue involved. Activation of immune cells and pro-inflammatory signaling has historically been considered an exclusively host-protective response that a pathogen would seek to avoid. However, recent advances in human and animal models suggest that in some tissues, GAS will activate and manipulate specific pro-inflammatory pathways to promote growth, nutrient acquisition, persistence, recurrent infection, competition with other microbial species, dissemination, and transmission. This review discusses molecular interactions between the host and pathogen to summarize how infection varies across tissue and stages of inflammation. A need for inflammation for GAS survival during common, mild infections may drive selection for mechanisms that cause pathological and excess inflammation severe diseases such as toxic shock syndrome, necrotizing fasciitis, and rheumatic heart disease.

A 族链球菌 (GAS) 在人类中具有极其广泛的组织趋向性，根据菌株的毒力因子库和所涉及的组织，表现为不同的疾病。免疫细胞的激活和促炎信号传导历来被认为是病原体试图避免的唯一宿主保护反应。然而，人类和动物模型的最新进展表明，在某些组织中，GAS 将激活和操纵特定的促炎途径，以促进生长、营养获取、持久性、反复感染、与其他微生物物种的竞争、传播和传播。这篇综述讨论了宿主和病原体之间的分子相互作用，以总结感染在组织和炎症阶段之间的变化。在常见的轻度感染期间，GAS 生存所需的炎症可能会推动对引起病理性和过度炎症的严重疾病（例如中毒性休克综合征、坏死性筋膜炎和风湿性心脏病）的机制的选择。