Innate response to self-antigen significantly exacerbates burn wound depth

doi:10.1073/pnas.0609026104

Innate response to self-antigen significantly exacerbates burn wound depth

*Harvard Medical School, Boston, MA 02115;
^†Department of Surgery, Brigham and Women's Hospital, Boston, MA 02115; and
^‡Departments of Pathology and Pediatrics, CBR Institute for Biomedical Research, Boston, MA 02115

Edited by Douglas T. Fearon, University of Cambridge, Cambridge, United Kingdom, and approved January 11, 2007 (received for review October 12, 2006)

Abstract

A major component of burn injury is caused by additional local damage from acute inflammation. Using a scald burn model in mice, we find that this part of the injury is dependent on recognition of self-antigen by specific natural IgM, leading to activation of the complement system. We propose that the depth of a burn wound is a sum of the thermal energy applied and of the degree of host inflammatory response.

Footnotes

^§To whom correspondence should be addressed. E-mail: fmoore{at}partners.org
Author contributions: F.S. and F.D.M. designed research; F.S. performed research; F.S. contributed new reagents/analytic tools; F.S., M.C.C., and F.D.M. analyzed data; and F.S., M.C.C., and F.D.M. wrote the paper.
Conflict of interest statement: M.C.C. and F.D.M. declare a potential financial interest. M.C.C. and F.D.M. are cofounders of DecImmune, Inc. DecImmune is licensed to develop therapeutics from N2 peptide and IgM^CM-22.
This article is a PNAS direct submission.
This article contains supporting information online at www.pnas.org/cgi/content/full/0609026104/DC1.
Abbreviation:

IR,

ischemia and reperfusion.