Innate immunity

NOD mice have a severly impaired ability to recruit leukocytes into sites of inflammation

  1. Gerben Bouma1,*,
  2. Tatjana Nikolic1,
  3. Jojanneke M. C. Coppens1,
  4. Cornelia G. van Helden-Meeuwsen1,
  5. Pieter J. M. Leenen1,
  6. Hemmo A. Drexhage1,
  7. Silvano Sozzani2,
  8. Marjan A. Versnel1

Article first published online: 9 DEC 2004

DOI: 10.1002/eji.200425513

Issue

European Journal of Immunology

European Journal of Immunology

Volume 35, Issue 1, pages 225–235, January 2005

Additional Information

How to Cite

Bouma, G., Nikolic, T., Coppens, J., van Helden-Meeuwsen, C., Leenen, P., Drexhage, H., Sozzani, S. and Versnel, M. (2005), NOD mice have a severly impaired ability to recruit leukocytes into sites of inflammation. European Journal of Immunology, 35: 225–235. doi: 10.1002/eji.200425513

Author Information

  1. 1

    Department of Immunology, Erasmus MC, Rotterdam, The Netherlands

  2. 2

    Section of General Pathology and Immunology, University of Brescia, Brescia, Italy

*Erasmus MC, Department of Immunology, Dr. Molewaterplein 50, 3015 GE Rotterdam, The Netherlands, Fax: +31–10–4089456

Publication History

  1. Issue published online: 16 DEC 2004
  2. Article first published online: 9 DEC 2004
  3. Manuscript Accepted: 8 NOV 2004
  4. Manuscript Revised: 2 NOV 2004
  5. Manuscript Received: 28 JUL 2004

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Keywords:

  • Monocytes;
  • NOD;
  • Migration;
  • Chemokines;
  • IL-10

Abstract

The accumulation of macrophages (MΦ) and dendritic cells (DC) in the pancreas plays a crucial role in the pathogenesis of autoimmune diabetes. We studied the recruitment of monocytes, MΦ and DC to sites of inflammation, i.e. the peritoneal cavity and a subcutaneously elicited air pouch in the NOD mouse model of autoimmune diabetes. The leukocyte recruitment was studied from 1 to 7 days after injection of thioglycollate (peritoneum), C5a (peritoneum, air pouch), CCL2 and CCL3 (air pouch). C57BL/6 and BALB/c mice served as controls. Morphological and flow cytometric analysis of the recruited cells was performed, IL-1β, TNF-α, IL-6, IL-12 and IL-10 in exudates measured, and in vitro CCL2-chemotaxis of exudate MΦ (Boyden chamber) determined. NOD mice were strongly impaired in the recruitment of MΦ, DC, monocytes, and granulocytes. Chemokine-injected air pouches of NOD mice showed an increased IL-10 and a decreased IL-1β level, while the other cytokines were normally or very lowly expressed. In addition, NOD exudate MΦ displayed an impaired in vitro CCL2-induced migration. Our data show that NOD mice have an impaired ability to recruit leukocytes into sites of inflammation elicited in the peritoneum and the air pouch. A raised IL-10/IL-1β ratio at these sites and a deficient migratory capacity of NOD monocytes are important determinants in this impairment.

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