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Updated: May 26, 2026

Detecting Migration and Infiltration of Neutrophils in Mice
10:33

Detecting Migration and Infiltration of Neutrophils in Mice

Published on: February 6, 2020

Regulation of the inflammatory response: enhancing neutrophil infiltration under chronic inflammatory conditions

Zhen Bian1, YaLan Guo, Binh Ha

  • 1Program of Cellular Biology and Immunology, Department of Biology, Georgia State University, Atlanta, GA 30303, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|December 14, 2011
PubMed

Insights

Neutrophil infiltration, crucial in inflammation, is amplified during chronic conditions like colitis. Interleukin-17A (IL-17A) drives this enhanced response, contributing to tissue damage.

Area of Science:

  • Immunology
  • Inflammation Research
  • Cellular Biology

Background:

  • Neutrophil (polymorphonuclear leukocyte [PMN]) infiltration is central to inflammation and tissue damage.
  • Controlling PMN infiltration is critical for managing inflammatory conditions.

Purpose of the Study:

  • To investigate the mechanisms underlying enhanced PMN infiltration during systemic inflammation.
  • To identify key molecular mediators involved in amplified PMN responses.

Main Methods:

  • Utilized a zymosan-induced peritonitis model in mice with systemic inflammation (colitis, diabetes).
  • Employed adoptive transfer experiments to assess the roles of circulating PMN and tissue macrophages.
  • Analyzed cellular and molecular changes in dextran sulfate sodium-induced colitis, focusing on IL-17A levels and cell function.
  • Conducted in vitro and ex vivo studies on isolated PMN and macrophages.

Main Results:

  • PMN response and infiltration were significantly enhanced in mice with systemic inflammation.
  • Both circulating PMN and tissue macrophages were altered, collectively contributing to increased PMN infiltration.
  • Enhanced PMN infiltration and macrophage function correlated with increased serum IL-17A during the postacute/chronic phase of colitis.
  • IL-17A directly modulated PMN and macrophage inflammatory responses in vitro and ex vivo.
  • IL-17A neutralization reduced PMN infiltration, IL-6 production, and prevented tissue damage in colitis models.

Conclusions:

  • IL-17A, produced during the chronic phase of colitis, acts as a feedback signal amplifying PMN infiltration.
  • Targeting IL-17A may be a therapeutic strategy to mitigate inflammation-driven tissue damage.

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