Innate response to self-antigen significantly exacerbates burn wound depth.
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.
Suber
Freeman
F
Harvard Medical School, Boston, MA 02115, USA.
Carroll
Michael C
MC
Moore
Francis D
FD
D000818:Animals; D001324:Autoantigens / Q000737:chemistry*; D002056:Burns / Q000378:metabolism*; D003181:Complement C4 / Q000235:genetics; D003165:Complement System Proteins / Q000378:metabolism*; D018398:Homeodomain Proteins / Q000235:genetics; D007075:Immunoglobulin M / Q000737:chemistry; D007249:Inflammation; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D010455:Peptides / Q000737:chemistry; D014945:Wound Healing; D014946:Wound Infection
D001324:Autoantigens; D003181:Complement C4; D018398:Homeodomain Proteins; D007075:Immunoglobulin M; D010455:Peptides; C064658:RAG-1 protein; D003165:Complement System Proteins