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• W1979801419 endingPage "e84479" @default.
• W1979801419 startingPage "e84479" @default.
• W1979801419 abstract "Acute kidney injury (AKI) is a common complication during systemic inflammatory response syndrome (SIRS), a potentially deadly clinical condition characterized by whole-body inflammatory state and organ dysfunction. CD44 is a ubiquitously expressed cell-surface transmembrane receptor with multiple functions in inflammatory processes, including sterile renal inflammation. The present study aimed to assess the role of CD44 in endotoxic shock-induced kidney inflammation and dysfunction by using CD44 KO and WT mice exposed intraperitoneally to LPS for 2, 4, and 24 hours . Upon LPS administration, CD44 expression in WT kidneys was augmented at all time-points. At 2 and 4 hours, CD44 KO animals showed a preserved renal function in comparison to WT mice. In absence of CD44, the pro-inflammatory cytokine levels in plasma and kidneys were lower, while renal expression of the anti-inflammatory cytokine IL-10 was higher. The cytokine levels were associated with decreased leukocyte influx and endothelial activation in CD44 KO kidneys. Furthermore, in vitro assays demonstrated a role of CD44 in enhancing macrophage cytokine responses to LPS and leukocyte migration. In conclusion, our study demonstrates that lack of CD44 impairs the early pro-inflammatory cytokine response to LPS, diminishes leukocyte migration/chemotaxis and endothelial activation, hence, delays endotoxic shock-induced AKI." @default.
• W1979801419 created "2016-06-24" @default.
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• W1979801419 date "2013-12-23" @default.
• W1979801419 modified "2023-10-13" @default.
• W1979801419 title "CD44-Deficiency Attenuates the Immunologic Responses to LPS and Delays the Onset of Endotoxic Shock-Induced Renal Inflammation and Dysfunction" @default.
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• W1979801419 doi "https://doi.org/10.1371/journal.pone.0084479" @default.
• W1979801419 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3871539" @default.
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