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Role of Polymorphonuclear Neutrophils on Infectious Complications Stemming from Enterococcus faecalis Oral Infection in Thermally Injured Mice¹

Yasuhiro Tsuda^*, Kenji Shigematsu^*, Makiko Kobayashi^*,, David N. Herndon and Fujio Suzuki^2,*,

^* Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX 77555; and Shriners Hospitals for Children, Galveston, TX 77550

Thermally injured mice are susceptible to Enterococcus faecalis translocation. In this study, the role of polymorphonuclear neutrophils (PMN) on the development of sepsis stemming from E. faecalis translocation was studied in SCID-beige (SCIDbg) mice depleted of PMN (SCIDbgN mice) or macrophages (M) and PMN (SCIDbgMN mice). Sepsis was not developed in SCIDbgN mice orally infected with E. faecalis, while the orally infected pathogen spread systemically in the same mice inoculated with PMN from thermally injured mice (TI-PMN). SCIDbgMN mice were shown to be greatly susceptible to sepsis caused by E. faecalis translocation, while orally infected E. faecalis did not spread into sepsis in the same mice that were previously inoculated with M from unburned SCIDbg mice (resident M). In contrast, orally infected E. faecalis spread systemically in SCIDbgMN mice inoculated with resident M and TI-PMN, while all SCIDbgMN mice inoculated in combination with resident M and PMN from unburned SCIDbg mice survived after the infection. After cultivation with TI-PMN in a dual-chamber transwell, resident M converted to alternatively activated M, which are inhibitory on the generation of classically activated M (typical effector cells in host antibacterial innate immunities). TI-PMN were characterized as immunosuppressive PMN (PMN-II) with abilities to produce cc-chemokine ligand-2 and IL-10. These results indicate that PMN-II appearing in response to burn injury impair host antibacterial resistance against sepsis stemming from E. faecalis translocation through the conversion of resident M to alternatively activated M.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Shriners of North American Grant 8840 (to F.S.).

² Address correspondence and reprint requests to Dr. Fujio Suzuki, Department of Internal Medicine, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555. E-mail address: fsuzuki{at}utmb.edu

³ Abbreviations used in this paper: PMN, polymorphonuclear neutrophil; M, macrophage; M1M, classically activated M; SCIDbg, SCID-beige mice; TI-PMN, PMN from thermally injured SCIDbg mice; M2M, alternatively activated M; SCIDbgN mice, SCIDbg mice depleted of PMN; SCIDbgMN mice, SCIDbgN mice depleted of M; iNOS, inducible NO synthase; SAC, Staphylococcus aureus Cowan I.