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Published online before print May 3, 2004

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(Journal of Leukocyte Biology. 2004;76:368-373.)
© 2004 by Society for Leukocyte Biology

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 and Fujio Suzuki^*,,1

^* Department of Internal Medicine, The University of Texas Medical Branch, Galveston;
Shriners Hospitals for Children, Galveston, Texas; and
First Department of Internal Medicine, Osaka Medical College, Takatsuki, Japan

¹Correspondence: The University of Texas Medical Branch, Department of Internal Medicine, 301 University Boulevard, Galveston, TX 77555-0435. E-mail: fsuzuki{at}utmb.edu

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 (RM) cultured with SIRS mouse sera converted to alternatively activated macrophages (AAM), which were also demonstrated in mice treated with recombinant murine CCL2. However, AAM 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 AAM generated from RM in response to SIRS-associated CCL2 production.

Key Words: SIRS • CCL2 • neutrophils • infectious complications

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