Despite advances in medicine, infectious diseases remain major causes of death and disability worldwide. Acute or chronic infectious agents mediate host tissue damage and cause a spectrum of disease as diverse as overwhelming sepsis and shock within hours to persistent tissue inflammation causing organ failure or even cancer over years. Although pathogen exposure can cause disease via host-derived inflammation, pathogens share recognized elements with harmless human commensals. Mouse models and organisms with simpler flora are revealing the dialogue between multicellular hosts and commensal flora. In some instances the persistent inflammation associated with pathogens can be interpreted within a framework of frustrated commensalism in which the host and pathogen cannot complete the requisite dialogue that establishes homeostasis. In contrast, coevolved commensals interact cooperatively with the host immune system, resulting in immunotolerance. Attempts to more thoroughly understand the molecular nature of the dialogue may uncover novel approaches to the control of inflammation and tissue damage.

中文翻译：

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传染性（非）耐受——沮丧的共生主义出了差错？

尽管医学取得了进步，传染病仍然是全世界死亡和残疾的主要原因。急性或慢性感染因子会介导宿主组织损伤，并引起一系列疾病，从数小时内发生的严重败血症和休克，到持续数年导致器官衰竭甚至癌症的持续组织炎症。尽管病原体暴露可通过宿主源性炎症引起疾病，但病原体与无害的人类共生体共享公认的元素。小鼠模型和具有更简单菌群的生物体揭示了多细胞宿主和共生菌群之间的对话。在某些情况下，与病原体相关的持续炎症可以在共生主义受挫的框架内解释，其中宿主和病原体无法完成建立体内平衡所必需的对话。相反，共同进化的共生体与宿主免疫系统相互作用，产生免疫耐受。尝试更彻底地了解对话的分子本质可能会发现控制炎症和组织损伤的新方法。