Webbläsaren som du använder stöds inte av denna webbplats. Alla versioner av Internet Explorer stöds inte längre, av oss eller Microsoft (läs mer här: * https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Var god och använd en modern webbläsare för att ta del av denna webbplats, som t.ex. nyaste versioner av Edge, Chrome, Firefox eller Safari osv.

Slit2 Prevents Neutrophil Recruitment and Renal Ischemia-Reperfusion Injury : english

In English

Författare

  • Swasti Chaturvedi
  • Darren A. Yuen
  • Amandeep Bajwa
  • Yi-Wei Huang
  • Christiane Sokollik
  • Liping Huang
  • Grace Y. Lam
  • Soumitra Tole
  • Guang-Ying Liu
  • Jerry Pan
  • Lauren Chan
  • Yaro Sokolskyy
  • Manoj Puthia
  • Gabriela Godaly
  • Rohan John
  • Changsen Wang
  • Warren L. Lee
  • John H. Brumell
  • Mark D. Okusa
  • Lisa A. Robinson
Visa allt

Summary, in English

Neutrophils recruited to the postischemic kidney contribute to the pathogenesis of ischemia-reperfusion injury (IRI), which is the most common cause of renal failure among hospitalized patients. The Slit family of secreted proteins inhibits chemotaxis of leukocytes by preventing activation of Rho-family GTPases, suggesting that members of this family might modulate the recruitment of neutrophils and the resulting IRI. Here, in static and microfluidic shear assays, Slit2 inhibited multiple steps required for the infiltration of neutrophils into tissue. Specifically, Slit2 blocked the capture and firm adhesion of human neutrophils to inflamed vascular endothelial barriers as well as their subsequent transmigration. To examine whether these observations were relevant to renal IRI, we administered Slit2 to mice before bilateral clamping of the renal pedicles. Assessed at 18 hours after reperfusion, Slit2 significantly inhibited renal tubular necrosis, neutrophil and macrophage infiltration, and rise in plasma creatinine. In vitro, Slit2 did not impair the protective functions of neutrophils, including phagocytosis and superoxide production, and did not inhibit neutrophils from killing the extracellular pathogen Staphylococcus aureus. In vivo, administration of Slit2 did not attenuate neutrophil recruitment or bacterial clearance in mice with ascending Escherichia coli urinary tract infections and did not increase the bacterial load in the livers of mice infected with the intracellular pathogen Listeria monocytogenes. Collectively, these results suggest that Slit2 may hold promise as a strategy to combat renal IRI without compromising the protective innate immune response.

Publiceringsår

2013

Språk

Engelska

Sidor

1274-1287

Publikation/Tidskrift/Serie

Journal of the American Society of Nephrology

Volym

24

Issue

8

Dokumenttyp

Artikel i tidskrift

Förlag

American Society of Nephrology

Ämne

  • Urology and Nephrology

Status

Published

ISBN/ISSN/Övrigt

  • ISSN: 1046-6673