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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0409235

Received for publication April 7, 2009.
Revised June 9, 2009.
Accepted for publication June 12, 2009.

Article

Enterococcus faecalis translocation in mice with severe burn injury: a pathogenic role of CCL2 and alternatively activated macrophages (M2aM{phi} and M2cM{phi})

Kenji Shigematsu *, Akira Asai *, Makiko Kobayashi *{dagger}, David N. Herndon {dagger}, and Fujio Suzuki *{dagger}@

*Department of Internal Medicine, The University of Texas Medical Branch, Galveston, Texas, USA; and{dagger}Shriners Hospitals for Children, Galveston, Texas, USA

@ To whom correspondence should be addressed. E-mail: fsuzuki{at}utmb.edu.


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Abstract

Here, we investigated a role of CCL2 on the increased susceptibility of severely burned mice to Enterococcus faecalis translocation. After inoculation of M{phi} from MLM{phi} of normal mice, 80% of the SCIDbgMN mice orally infected with the lethal dose of E. faecalis survived, and all mice inoculated with MLM{phi} from thermally injured mice died. At this time, SCIDbgMN mice inoculated with MLM{phi} from thermally injured CCL2-/- mice were shown to be resistant (90% survival). M1M{phi} were not induced by E. faecalis antigen in cultures of MLM{phi} from thermally injured wild-type mice, and MLM{phi} from thermally injured CCL2-/- mice converted to M1M{phi} after the antigen stimulation. MLM{phi} from wild-type mice 2 days postburn injury possessed M2a- and M2cM{phi} properties, and those from mice 7–21 days postburn injury carried M2bM{phi} properties. However, MLM{phi} from thermally injured CCL2-/- mice did not show any typical properties for M2a- or M2cM{phi}. CCL17 and CXCL13 (biomarkers for M2a- and M2cM{phi}), but not CCL1 (a biomarker of M2bM{phi}), were produced by MLM{phi} from thermally injured CCL2-/- mice treated with rCCL2. These results indicate that CCL2 converts resident MLM{phi} to M2a- and M2cM{phi}, detected early after burn injury, and decreases host antibacterial innate immunity against sepsis stemming from oral E. faecalis infection.

Key Words: enterococci • thermal injury