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ABSTRACT: Effects of KP on bacterial community (pot)

PROVIDER: PRJNA625525 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11553676_1.fastq.gz	Fastqsanger.gz
	SRR11553676_2.fastq.gz	Fastqsanger.gz
	SRR11553677_1.fastq.gz	Fastqsanger.gz
	SRR11553677_2.fastq.gz	Fastqsanger.gz
	SRR11553678_1.fastq.gz	Fastqsanger.gz

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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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C. elegans genomic response to Konza Prairie Soil bacterial environment

Project description:Here we have compared adult wildtype (N2) C. elegans gene expression when grown on different bacterial environments/fod sources in an effort to model naturally occuring nematode-bacteria interactions at the Konza Prairie. We hypothesize that human-induced changes to natural environments, such as the addition of nitrogen fertalizer, have effects on the bacterial community in soils and this drives downstream changes in the structure on soil bacterial-feeding nematode community structure. Here we have used transcriptional profiling to identify candidate genes involved in the interaction of nematodes and bacteria in nature.

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