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IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota [scRNA-seq]

ABSTRACT: IL-22 plays a critical role in defending against mucosal infections, but how IL-22 production is regulated is incompletely understood. Here, we show that mice lacking IL-33 or its receptor ST2 (IL-1RL1) were more resistant to Streptococcus pneumoniae lung infection than wild-type animals, and that single nucleotide polymorphisms in IL33 and IL1RL1 were associated with pneumococcal pneumonia in humans. The effect of IL-33 on S. pneumoniae infection was mediated by negative regulation of IL-22 production by innate lymphoid cells (ILCs), but independent of ILC2s as well as IL-4 and IL-13 signaling. Moreover, IL-33´s influence on antibacterial defense was dependent on housing conditions of the mice, and mediated by the modulatory effect of IL-33 on the intestinal microbiota. Collectively, we reveal that IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota. Our study thus provides insight into the bidirectional crosstalk between the innate immune system and the microbiota and how it shapes susceptibility to bacterial infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE236342 | GEO | 2024/03/19

REPOSITORIES: GEO

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IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota [shotgun sequencing]

Project description:IL-22 plays a critical role in defending against mucosal infections, but how IL-22 production is regulated is incompletely understood. Here, we show that mice lacking IL-33 or its receptor ST2 (IL-1RL1) were more resistant to Streptococcus pneumoniae lung infection than wild-type animals, and that single nucleotide polymorphisms in IL33 and IL1RL1 were associated with pneumococcal pneumonia in humans. The effect of IL-33 on S. pneumoniae infection was mediated by negative regulation of IL-22 production by innate lymphoid cells (ILCs), but independent of ILC2s as well as IL-4 and IL-13 signaling. Moreover, IL-33´s influence on antibacterial defense was dependent on housing conditions of the mice, and mediated by the modulatory effect of IL-33 on the intestinal microbiota. Collectively, we reveal that IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota. Our study thus provides insight into the bidirectional crosstalk between the innate immune system and the microbiota and how it shapes susceptibility to bacterial infection.

2024-03-19 | GSE236343 | GEO

IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota [bulk RNA-seq]

Project description:IL-22 plays a critical role in defending against mucosal infections, but how IL-22 production is regulated is incompletely understood. Here, we show that mice lacking IL-33 or its receptor ST2 (IL-1RL1) were more resistant to Streptococcus pneumoniae lung infection than wild-type animals, and that single nucleotide polymorphisms in IL33 and IL1RL1 were associated with pneumococcal pneumonia in humans. The effect of IL-33 on S. pneumoniae infection was mediated by negative regulation of IL-22 production by innate lymphoid cells (ILCs), but independent of ILC2s as well as IL-4 and IL-13 signaling. Moreover, IL-33´s influence on antibacterial defense was dependent on the housing conditions of the mice, and mediated by IL-33´s modulatory effect on the intestinal microbiota. Collectively, we reveal that IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota. Our study thus provides insight into the bidirectional crosstalk between the innate immune system and the microbiota and how it shapes susceptibility to bacterial infection.

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IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota.

Project description:IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota.

| PRJNA990658 | ENA

IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota [scRNA-seq]

Project description:IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota [scRNA-seq]

| PRJNA990666 | ENA

IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota [shotgun sequencing]

Project description:IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota [shotgun sequencing]

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IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota [bulk RNA-seq]

Project description:IL-33 controls IL-22-dependent antibacterial defense by modulating the microbiota [bulk RNA-seq]

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RNA-seq of mouse ileum to investigate the role of IL-17 receptor signaling in Paneth cells in their biology and intestinal physiology

Project description:IL-17 receptor plays a major role in the antibacterial defense and regulation of host-microbiota interaction. However its impact on Paneth cells, cell-type specific for production of antibacterial peptides, is still not clear. Here, we used genetic depletion of IL-17 receptor specific for Paneth cell population (Defa6-iCre x Il17ra-flox) and performed the RNA sequencing on FACS-sorted Paneth cells and also complete ileum tissue, comparing Cre+ and Cre- littermates.

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Project description:Hypervirulent epidemic strains of Clostridium difficile (C. difficile), referred to as NAPI/027, express an additional virulence factor, binary toxin (CDT), and are associated with more severe disease. Emerging evidence indicates gut immunity to C. difficile is a delicate balance between protection and pathology. To identify potential therapeutic host immune targets, we conducted a transcriptome analysis of host genes altered by NAPI/027 infection and identified interleukin-33 (IL-33) as a candidate immune target. Using a murine model, we show that both endogenous IL-33 and exogenous IL-33 treatment protect from the enhanced mortality, weight-loss and tissue pathology which is characteristic of hypervirulent C. difficile. IL-33 mediated protection was elicited through type-2 innate lymphoid cells (ILC2s) and adoptive transfer of purified ILC2s was sufficient to mitigate CDI- associated mortality and weight-loss. Furthermore, dysregulated IL-33 signaling via the soluble IL-33 decoy receptor (sST2) predicted disease severity and mortality in human patients. Lastly, colonic IL-33 expression appears to be regulated by the microbiota as antibiotic- depletion of IL-33 was rescued with mouse fecal microbiota transplant (FMT) and a human fecal spore preparation (HSP). Thus, IL-33 signaling is a novel therapeutic pathway for severe CDI which can potentially be targeted with rationally designed microbial therapies.

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Transcription profiling of IL-22-/- samples

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