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Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine
09:25

Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine

Published on: May 21, 2012

The Nod2 sensor promotes intestinal pathogen eradication via the chemokine CCL2-dependent recruitment of inflammatory

Yun-Gi Kim1, Nobuhiko Kamada, Michael H Shaw

  • 1Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

Immunity
|May 14, 2011
PubMed

Insights

The Nod2 sensor is crucial for intestinal defense against bacteria. Its deficiency impairs the recruitment of monocytes, essential for clearing infections like Citrobacter rodentium.

Area of Science:

  • Immunology
  • Microbiology
  • Gastroenterology

Background:

  • The Nod2 sensor plays a role in host defense against bacteria.
  • Nod2 dysfunction is linked to Crohn's disease, but its precise function is unclear.

Purpose of the Study:

  • To investigate the role of Nod2 in intestinal host defense against enteric bacterial infection.

Main Methods:

  • Utilized Nod2 knockout (Nod2-/-) mice and Citrobacter rodentium infection model.
  • Assessed chemokine production, immune cell recruitment (monocytes, Th1 cells), and bacterial clearance.
  • Investigated CCL2 production by different cell types and the role of monocytes via adoptive transfer.

Main Results:

  • Nod2-/- mice showed impaired intestinal clearance of Citrobacter rodentium.
  • Reduced CCL2 chemokine production and inflammatory monocyte recruitment were observed in Nod2-/- mice.
  • Colonic stromal cells produced CCL2 in a Nod2-dependent manner, while inflammatory monocytes produced IL-12, crucial for adaptive immunity.

Conclusions:

  • Nod2 signaling is essential for CCL2-dependent recruitment of inflammatory monocytes to the intestine.
  • This monocyte recruitment promotes bacterial eradication, highlighting a key mechanism in intestinal host defense.

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