Published online before print March 27, 2008

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(Journal of Leukocyte Biology. 2008;83:1354-1362.)
© 2008 by Society for Leukocyte Biology

Gr-1⁺CD11b⁺ cells as an accelerator of sepsis stemming from Pseudomonas aeruginosa wound infection in thermally injured mice

Makiko Kobayashi^*,, Tsuyoshi Yoshida^*, Dan Takeuchi^*, Vickie C. Jones^*, Kenji Shigematsu^*, David N. Herndon and Fujio Suzuki^*,,1

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

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

ABSTRACT

Using a mouse model of thermal injury, we studied why antimicrobial peptides are not produced at the burn-site tissues and how this defect contributes to the increased susceptibility to Pseudomonas aeruginosa burn-wound infection. Logarithmic growth of P. aeruginosa was demonstrated locally (at the burn site) and systemically (in circulation) in thermally injured mice exposed to 10² CFU/mouse of the pathogen beneath the burn wound. However, neither systemic nor local growth of the pathogen was observed in sham burn mice when they were infected intradermally with 10⁶ CFU/mouse P. aeruginosa. Murine β-defensins (MBDs) were detected in the skin homogenates of sham burn mice. However, the amounts of MBDs were reduced greatly in the same tissue homogenates from thermally injured mice. Gr-1⁺CD11b⁺ cells, with an ability to suppress antimicrobial peptide production by skin keratinocytes, were isolated from tissues surrounding the burn areas, and these cells were not obtained from skin tissues of sham burn mice. After intradermal inoculation of Gr-1⁺CD11b⁺ cells, which were isolated from burn-site tissues, the production of antimicrobial peptides around the cell-inoculation site of sham burn mice decreased. Also, like thermally injured mice, these mice were shown to be susceptible to P. aeruginosa intradermal infection. These results indicate that sepsis stemming from P. aeruginosa burn-wound infection is accelerated by burn-induced Gr-1⁺CD11b⁺ cells with abilities to suppress antimicrobial peptide production by epidermal keratinocytes.

Key Words: thermal injury • β-defensin

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