Altered neutrophil trafficking during sepsis.

  • Guo R
  • Riedemann N
  • Laudes I
 et al. 
  • 19


    Mendeley users who have this article in their library.
  • 53


    Citations of this article.


In sepsis, dysregulation of the inflammatory system is well known, as reflected in excessive inflammatory mediator production, complement activation, and appearance of defects in phagocytic cells. In the current study sepsis was induced in rats by cecal ligation/puncture. Early in sepsis the beta(1) and beta(2) integrin content on blood neutrophils increased in a nontranscriptional manner, and the increase in beta(2), but not beta(1), integrin content was C5a dependent. Similar changes could be induced in vitro on blood neutrophils following contact with phorbol ester or C5a. Direct injury of lungs of normal rats induced by deposition of IgG immune complexes (IgG-IC) caused 5-fold increases in the myeloperoxidase content that was beta(2), but not beta(1), dependent. In contrast, in cecal ligation/puncture lungs myeloperoxidase increased 10-fold after IgG immune complex deposition and was both beta(1) and beta(2) integrin dependent. These data suggest that sepsis causes enhanced neutrophil trafficking into the lung via mechanisms that are not engaged in the nonseptic state.

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document


  • Ren-Feng Guo

  • Niels C Riedemann

  • Ines J Laudes

  • Vidya J Sarma

  • Robin G Kunkel

  • Kari a Dilley

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free