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Psychological stress increases susceptibility to Staphylococcus aureus infection by the action of TGFβ to suppress immune acting fibroblasts [scRNA-Seq]

ABSTRACT: Psychological stress increases susceptibility to Staphylococcus aureus infection by the action of TGFβ to suppress immune acting fibroblasts [scRNA-Seq]

PROVIDER: PRJNA1128061 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR29543006_1.fastq.gz	Fastqsanger.gz
	SRR29543006_2.fastq.gz	Fastqsanger.gz
	SRR29543007_1.fastq.gz	Fastqsanger.gz
	SRR29543007_2.fastq.gz	Fastqsanger.gz

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Psychological stress increases susceptibility to Staphylococcus aureus infection by the action of TGFβ to suppress immune acting fibroblasts [RNA-Seq]

Project description:Psychological stress results in increased susceptibility to infection yet the mechanisms responsible for this major healthcare burden are incompletely understood. In mice, stress induced by restraint increases infection by Staphylococcus aureus while adrenalectomy or chemical inhibition of adrenergic signaling blocks this response. Single-cell transcriptomics and lipidomic profiling of the skin after stress reveal fibroblasts undergoing adipogenesis are the major cell type responding to stress. Fibroblasts are critical to the increase in infection as adrenaline inhibits fibroblast Camp expression and bacterial killing, and stress did not increase infection in mice that lack Camp in fibroblasts. The suppression of the antimicrobial function of Camp in fibroblasts occurs due to activation of TGFβ signaling and is critical to the capacity of stress to increase susceptibility to infection since treatment of mice with a neutralizing TGFβ antibody or a TGFβ receptor inhibitor restores expression of Camp and alleviates increased susceptibility to infection. These data show that susceptibility to infection after psychological stress is due to a brain-skin axis that induces TGFβ and subsequently inhibits host defense by immune acting fibroblasts in the dermis. This identifies TGFβ as an unexpected target that can ameliorate increased bacterial infections associated with stress.

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Psychological stress increases susceptibility to Staphylococcus aureus infection by the action of TGFβ to suppress immune acting fibroblasts [scRNA-Seq]

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Psychological stress increases susceptibility to Staphylococcus aureus infection by the action of TGFβ to suppress immune acting fibroblasts [RNA-Seq]

Project description:Psychological stress increases susceptibility to Staphylococcus aureus infection by the action of TGFβ to suppress immune acting fibroblasts [RNA-Seq]

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Project description:Recent studies have been successful at utilizing ectopic expression of transcription factors to generate induced cardiomyocytes (iCMs) from fibroblasts, albeit at a low frequency in vitro. This work investigates the influence of small molecules that have been previously reported to improve differentiation to cardiomyocytes as well as reprogramming to iPSCs in conjunction with ectopic expression of the transcription factors Hand2, Nkx2.5, Gata4, Mef2C, and Tbx5 on the conversion to functional iCMs. We utilized a reporter system in which the calcium indicator GCaMP is driven by the cardiac Troponin T promoter to quantify iCM yield. The TGFβ inhibitor, SB431542 (SB), was identified as a small molecule capable of increasing the conversion of both mouse embryonic fibroblasts and adult cardiac fibroblasts to iCMs up to ~5 fold. Further characterization revealed that inhibition of TGFβ by SB early in the reprogramming process led to the greatest increase in conversion of fibroblasts to iCMs in a dose-responsive manner. Global transcriptional analysis at Day 3 post-induction of the transcription factors revealed an increased expression of genes associated with the development of cardiac muscle in the presence of SB compared to the vehicle control. Incorporation of SB in the reprogramming process increases the efficiency of iCM generation, one of the major goals necessary to enable the use of iCMs for discovery-based applications and for the clinic. Mouse embryonic fibroblasts (MEFs) and adult mouse cardiac fibroblasts (CFs) were transfected with an empty vector (0F) or the combination of Hand2, Nkx2.5, Gata4, Mef2C, and Tbx5 (5F). Samples were exposed to the vehicle control (D, DMSO), SB431542 (SB, 0.5 uM MEF, 5 uM CF), or TGFb1 (T, 2 ng/mL) during culture. Transcription factor expression was induced at Day 0 and samples were isolated at Day 3 post-induction.

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