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摄入蜡样芽胞杆菌孢子会抑制免疫反应,有利于细菌的持续存在。

Ingestion of Bacillus cereus spores dampens the immune response to favor bacterial persistence.

机构信息

Université Côte d'Azur, CNRS, INRAE, ISA, Sophia Antipolis, France.

Université Côte d'Azur, Inserm, C3M, Nice, France.

出版信息

Nat Commun. 2024 Sep 4;15(1):7733. doi: 10.1038/s41467-024-51689-9.

Abstract

Strains of the Bacillus cereus (Bc) group are sporulating bacteria commonly associated with foodborne outbreaks. Spores are dormant cells highly resistant to extreme conditions. Nevertheless, the pathological processes associated with the ingestion of either vegetative cells or spores remain poorly understood. Here, we demonstrate that while ingestion of vegetative bacteria leads to their rapid elimination from the intestine of Drosophila melanogaster, a single ingestion of spores leads to the persistence of bacteria for at least 10 days. We show that spores do not germinate in the anterior part of the intestine which bears the innate immune defenses. Consequently, spores reach the posterior intestine where they germinate and activate both the Imd and Toll immune pathways. Unexpectedly, this leads to the induction of amidases, which are negative regulators of the immune response, but not to antimicrobial peptides. Thereby, the local germination of spores in the posterior intestine dampens the immune signaling that in turn fosters the persistence of Bc bacteria. This study provides evidence for how Bc spores hijack the intestinal immune defenses allowing the localized birth of vegetative bacteria responsible for the digestive symptoms associated with foodborne illness outbreaks.

摘要

蜡样芽胞杆菌(Bc)是一种形成孢子的细菌,通常与食源性疾病爆发有关。孢子是休眠细胞,对极端条件具有高度抗性。然而,与摄入营养细胞或孢子相关的病理过程仍知之甚少。在这里,我们证明了尽管摄入营养细菌会导致它们从黑腹果蝇的肠道中迅速消除,但单次摄入孢子会导致细菌至少持续存在 10 天。我们表明,孢子不会在具有先天免疫防御的肠前段发芽。因此,孢子到达后肠,在那里它们发芽并激活 Imd 和 Toll 免疫途径。出乎意料的是,这会诱导酰胺酶的产生,酰胺酶是免疫反应的负调节剂,但不是抗菌肽。因此,后肠中孢子的局部发芽会抑制免疫信号,从而促进 Bc 细菌的持续存在。这项研究提供了证据,证明 Bc 孢子如何劫持肠道免疫防御系统,从而使负责与食源性疾病爆发相关的消化症状的营养细菌在局部产生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3082/11375157/9d78722d6060/41467_2024_51689_Fig1_HTML.jpg

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