CCL2, a product of mice early after systemic inflammatory response syndrome (SIRS), induces alternatively activated macrophages capable of impairing antibacterial resistance of SIRS mice

Yasuhiro Tsuda, Hitoshi Takahashi, Makiko Kobayashi, Toshiaki Hanafusa, David N. Herndon, Fujio Suzuki

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

Infection associated with systemic inflammatory response syndrome (SIRS) is a major cause of morbidity and mortality in patients with major surgery, polytrauma, and severe burn injury. In previous studies, mice with severe pancreatitis (a mouse model of SIRS, SIRS mice) have been shown to be greatly susceptible to various infections. In the present study, a mechanism involved in the impaired resistance of SIRS mice to infectious complications was investigated. Sera from SIRS mice impaired the resistance of normal mice to infectious complications induced by cecal ligation and puncture (CLP). CC chemokine ligand 2 (CCL2) was detected in sera of SIRS mice. Resident macrophages (RMφ) cultured with SIRS mouse sera converted to alternatively activated macrophages (AAMφ), which were also demonstrated in mice treated with recombinant murine CCL2. However, AAMφ were not demonstrated in mice injected with SIRS mouse sera and anti-CCL2 monoclonal antibody (mAb) in combination. Furthermore, normal mice that received SIRS mouse sera and anti-CCL2 mAb resisted CLP-induced infectious complications. These results indicate that the resistance of SIRS mice to infectious complications is impaired by AMMφ generated from RMφ in response to SIRS-associated CCL2 production.

Original languageEnglish (US)
Pages (from-to)368-373
Number of pages6
JournalJournal of Leukocyte Biology
Volume76
Issue number2
DOIs
StatePublished - Aug 2004

Keywords

  • CCL2
  • Infectious complications
  • Neutrophils
  • SIRS

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology

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