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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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Project description:Bacterial community in switchgrass field

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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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Project description:Bacterial community diversity in potato field

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Project description:Bacterial community analysis in potato field

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Transcriptional Regulationand Chromatin Dynamics in Human Epithelial Cell Differentiation (ChIP-seq)

Project description:Genome-wide mapping of H3K4me1, H3K4me3 and H3K27ac in KP and DK ChIP-seq for H3K4me1, H3K4me3 and H3K27ac in KP and DK p63 profiling of DK through ChIP-seq

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16S rRNA community profiling of the gut of the African Palm weevil

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Project description:Mesiq sequencing of Bacterial community in maize field

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Effect of Batf2 deficiency on gene epxression in murine alveolar macrophages treated ex vivo with IFNg and K. pneumoniae supernatant

Project description:Basic leucine zipper transcription factor ATF-like 2 (BATF2) is a transcription factor that is emerging as an important regulator of the innate immune system. We previously identified BATF2 among the top upregulated genes in human alveolar macrophages treated with LPS, but the signaling pathways that induce BATF2 expression in response to Gram-negative stimuli are incompletely understood. In addition, the role of BATF2 in the host response to pulmonary infection with a Gram-negative pathogen like Klebsiella pneumoniae (Kp) is not known. We show that induction of Batf2 gene expression in macrophages in response to Kp in vitro requires TRIF and type I interferon (IFN) signaling, but not MyD88 signaling. Analysis of the impact of BATF2-deficiency on macrophage effector functions in vitro showed that BATF2 does not directly impact macrophage phagocytic uptake and intracellular killing of Kp. However, BATF2 markedly enhanced macrophage pro-inflammatory gene expression and Kp-induced cytokine responses. In vivo, we observed that Batf2 gene expression was elevated in the lung tissue of wild type (WT) mice 24 h after pulmonary Kp infection, and Kp-infected BATF2-deficient (Batf2-/-) mice displayed a modest but significant increase in bacterial burden in the lung, spleen and liver compared to WT mice. WT and Batf2-/- mice showed similar recruitment of leukocytes following infection, but in line with our in vitro observations, pro-inflammatory cytokine levels in the alveolar space were reduced in Batf2-/- mice. Altogether, these results suggest that BATF2 enhances pro-inflammatory cytokine responses in macrophages in response to Kp, and that as such, BATF2 contributes to the host defense against pulmonary Kp infection.

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