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ABSTRACT: Effects of KP on bacterial community (field)

PROVIDER: PRJNA625533 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11553700_1.fastq.gz	Fastqsanger.gz
	SRR11553700_2.fastq.gz	Fastqsanger.gz
	SRR11553701_1.fastq.gz	Fastqsanger.gz
	SRR11553701_2.fastq.gz	Fastqsanger.gz
	SRR11553702_1.fastq.gz	Fastqsanger.gz

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Project description:Effects of KP on bacterial community (pot)

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STAT1 employs myeloid cell-extrinsic mechanisms to regulate the neutrophil response and provide protection against invasive Klebsiella pneumoniae lung infection

Project description:Klebsiella pneumoniae (KP) are extracellular Gram-negative bacteria that cause infections in lower respiratory and urinary tract, and bloodstream. STAT1 is a master transcription factor that acts to maintain T-cell quiescence under homeostatic conditions. Although STAT1 helps defend against systemic spread of acute KP intrapulmonary infection, whether STAT1 regulation of T-cell homeostasis impacts pulmonary host defense during acute bacterial infection and injury is less clear. Using a clinical KP respiratory isolate and a pneumonia mouse model, we found STAT1-deficiency led to an early neutrophil-dominant transcriptional profile and neutrophil-recruitment in the lung preceding widespread bacterial dissemination and lung injury development. Yet, myeloid cell STAT1 was dispensable for control of KP proliferation and dissemination, as myeloid cell-specific STAT1-deficient (LysMCre/WT;Stat1fl/fl) mice showed similar bacterial burden in lung, liver, and kidney as WT littermates. Surprisingly, IL-17 producing CD4+ T-cells infiltrated Stat1-/- mice lungs early during KP infection. Increase in Th17-cells in the lung was not due to preexisting immunity against KP and were consistent with circulating rather than tissue-resident CD4+ T-cells. However, blocking global IL17 signaling with anti-IL17-RC administration led to increased proliferation and dissemination of KP, suggesting IL17 provided by other innate immune cells is essential in defense against KP. Contrastingly, depletion of CD4+ T-cells reduced Stat1-/- mice lung bacterial burden indicating early CD4+ T-cell activation in the setting of global STAT1-deficiency is pathogenic. Altogether, our findings suggest STAT1 employs myeloid cell-extrinsic mechanisms to regulate neutrophil responses and provide protection against invasive KP by restricting non-specific CD4+ T-cell activation and immunopathology in the lung.

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