关键词: Canonical Dysregulation Gut microbiota Inflammasome Non-canonical

Mesh : Humans Inflammasomes / metabolism Gastrointestinal Microbiome Cytokines / metabolism

来  源:   DOI:10.1186/s12964-024-01504-1   PDF(Pubmed)

Abstract:
Inflammasomes are complex platforms for the cleavage and release of inactivated IL-1β and IL-18 cytokines that trigger inflammatory responses against damage-associated molecular patterns (DAMPs) or pathogen-associated molecular patterns (PAMPs). Gut microbiota plays a pivotal role in maintaining gut homeostasis. Inflammasome activation needs to be tightly regulated to limit aberrant activation and bystander damage to the host cells. Several types of inflammasomes, including Node-like receptor protein family (e.g., NLRP1, NLRP3, NLRP6, NLRP12, NLRC4), PYHIN family, and pyrin inflammasomes, interact with gut microbiota to maintain gut homeostasis. This review discusses the current understanding of how inflammasomes and microbiota interact, and how this interaction impacts human health. Additionally, we introduce novel biologics and antagonists, such as inhibitors of IL-1β and inflammasomes, as therapeutic strategies for treating gastrointestinal disorders when inflammasomes are dysregulated or the composition of gut microbiota changes.
摘要:
炎性体是用于裂解和释放灭活的IL-1β和IL-18细胞因子的复杂平台,这些细胞因子引发针对损伤相关分子模式(DAMP)或病原体相关分子模式(PAMP)的炎症反应。肠道菌群在维持肠道稳态中起着关键作用。炎症小体激活需要严格调节以限制异常激活和对宿主细胞的旁观者损伤。几种类型的炎性体,包括节点样受体蛋白家族(例如,NLRP1,NLRP3,NLRP6,NLRP12,NLRC4),PYHIN家族,还有pyrin炎性体,与肠道微生物群相互作用以维持肠道稳态。这篇综述讨论了目前对炎性体和微生物群如何相互作用的理解,以及这种相互作用如何影响人类健康。此外,我们介绍新的生物制剂和拮抗剂,如IL-1β和炎性体的抑制剂,作为治疗胃肠道疾病的治疗策略,当炎性体失调或肠道微生物群的组成发生变化时。
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