MassIVE MSV000089030

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Vascular proteome responses precede organ dysfunction in a murine model of Staphylococcus aureus bacteremia

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Description

Vascular dysfunction and organ failure are two distinct, albeit highly interconnected clinical outcomes linked to morbidity and mortality in human sepsis. The mechanisms driving vascular and parenchymal damage are dynamic and display significant molecular crosstalk between organs and tissues. Therefore, assessing their individual contribution to disease progression is technically challenging. Here, we hypothesize that dysregulated vascular responses predispose the organism to organ failure. To address this hypothesis, we have evaluated four major organs in a murine model of S. aureus sepsis by combining in vivo labeling of the endothelial proteome, data-independent acquisition (DIA) mass spectrometry, and an integrative computational pipeline. The data reveal, with unprecedented depth and throughput, that a septic insult evokes organ-specific proteome responses that are highly compartmentalized, synchronously coordinated, and significantly correlated with the progression of the disease. This includes abundant vascular shedding, dysregulation of the intrinsic pathway of coagulation, compartmentalization of the acute phase-response, and abundant upregulation of glycocalyx components. Vascular proteome changes were also found to precede bacterial invasion and leukocyte infiltration into the organs, as well as to precede changes in various well-established cellular and biochemical correlates of systemic coagulopathy and tissue dysfunction. Importantly, our data suggests a potential role for the vascular proteome as a determinant of the susceptibility of the organs to undergo failure during sepsis. [doi:10.25345/C55717R51] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: Vascular glycocalyx ; Sepsis ; Proteomics ; Staphylococcus aureus

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Principal Investigators:
(in alphabetical order) 		Alejandro Gomez Toledo, Lund University, Sweden
Submitting User: alejandro1018
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