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Type II interferon-dependent antibacterial defense in the lungs is compromised in diabetes

ABSTRACT: Type II interferon-dependent antibacterial defense in the lungs is compromised in diabetes

PROVIDER: PRJNA1128018 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29546983_1.fastq.gz	Fastqsanger.gz
	SRR29546983_2.fastq.gz	Fastqsanger.gz
	SRR29546984_1.fastq.gz	Fastqsanger.gz
	SRR29546984_2.fastq.gz	Fastqsanger.gz
	SRR29546985_1.fastq.gz	Fastqsanger.gz

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Type II interferon-dependent antibacterial defense in the lungs is compromised in diabetes

Project description:Diabetes mellitus is associated with an increased risk of pneumonia, which is often caused by so-called typical and atypical pathogens including Streptoccocus pneumoniae and Legionella pneumophila, respectively. Here, we employed a varity of mouse models to investigate how diabetes influences pulmonary antibacterial immunity. Following intranasal infection with Streptoccocus pneumoniae or Legionella pneumphila, type 2 diabetic and prediabetic mice had higher bacterial loads in their lungs as compared to control animals. Single cell RNA sequencing, flow cytometry, and functional analyses revealed a compromised type II IFN (IFNg) production by natural killer cells in diabetic and prediabetic mice, which was linked to reduced IL-12 production by CD103+ dendritic cells. Treatment with IFNg rescued antibacterial defense against L. pneumophila but not against S. pneumoniae in diabetic animals, although impaired production of IFNg also contributed to the compromised anti-pneumococcal resistance in diabetic mice. These findings uncover a mechanism that could help to explain why type 2 diabetes predisposes to pneumonia. We establish proof of concept for host-directed treatment strategies to reinforce compromised IFNg-mediated antibacterial defense against atypical lung pathogens.

2024-11-19 | GSE270694 | GEO

An essential role for the antiviral endoribonuclease, RNase-L, in antibacterial immunity.

Project description:Type I interferons were discovered as the primary antiviral cytokines and are now known to serve critical functions in host defense against bacterial pathogens. Accordingly, established mediators of interferon antiviral activity may mediate previously unrecognized antibacterial functions. RNase-L is the terminal component of an RNA decay pathway that is an important mediator of interferon-induced antiviral activity. Here we identify a novel role for RNase-L in the host antibacterial response. RNase-L-/- mice exhibited a dramatic increase in mortality following challenge with Bacillus anthracis and Escherichia coli; this increased susceptibility was due to a compromised immune response resulting in increased bacterial load. Investigation of the mechanisms of RNase-L antibacterial activity indicated that RNase-L is required for the optimal induction of proinflammatory cytokines that play essential roles in host defense from bacterial pathogens. RNase-L also regulated the expression of the endolysosomal protease, cathepsin-E, and endosome-associated activities, that function to eliminate internalized bacteria and may contribute to RNase-L antimicrobial action. Our results reveal a unique role for RNase-L in the antibacterial response that is mediated through multiple mechanisms. As a regulator of fundamental components of the innate immune response, RNase-L represents a viable therapeutic target to augment host defense against diverse microbial pathogens. two strains: wildtype and knockout, three time points: untreated, 2hours, and 8hours. three replication for each group. Totally 18 samples.

2008-12-19 | E-GEOD-13530 | biostudies-arrayexpress

An essential role for the antiviral endoribonuclease, RNase-L, in antibacterial immunity.

2008-12-19 | GSE13530 | GEO

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.

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

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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 [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 [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 [bulk RNA-seq]

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