Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The . gov means it’s official. Federal government websites often end in . gov or . mil. Before sharing sensitive information, make sure you’re on a federal government site VSports app下载. .

Https

The site is secure V体育官网. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. .

. 2013 Dec;43(12):3306-13.
doi: 10.1002/eji.201343441. Epub 2013 Aug 29.

Apoptotic cells enhance sphingosine-1-phosphate receptor 1 dependent macrophage migration

Benjamin Weichand  1 , Nicole Weis, Andreas Weigert, Nina Grossmann, Bodo Levkau, Bernhard Brüne
Affiliations
Free article

Apoptotic cells enhance sphingosine-1-phosphate receptor 1 dependent macrophage migration

Benjamin Weichand et al. Eur J Immunol. 2013 Dec.
Free article

Abstract

The lipid sphingosine-1-phosphate (S1P) is a chemokine for a variety of immune cells including lymphocytes and monocytes VSports手机版. Migration toward S1P is determined by the S1P receptor expression profile, with S1PR1/3 (where S1PR is S1P receptor) stimulating and S1PR2 attenuating migration. However, the impact and physiological significance of S1P-induced migration of macrophages is largely unclear. We observed that alternative activation of human macrophages, by IL-4 or apoptotic cells (ACs), enhanced S1PR1 expression. Moreover, ACs provoked macrophage migration toward S1P in an S1PR1-dependent manner as confirmed by pharmacological receptor inhibition and S1PR1-deficient murine macrophages. In a mouse model of resolving peritoneal inflammation, F4/80-driven deletion of S1PR1 reduced postinflammatory macrophage emigration from inflammatory sites. S1PR1 expression on macrophages might, therefore, be relevant for restoring tissue homeostasis during the resolution of inflammation. .

Keywords: Macrophage activation; Peritonitis; Resolution of inflammation; Sphingolipids; Zymosan. V体育安卓版.

PubMed Disclaimer

Publication types

MeSH terms

LinkOut - more resources