Burn induces a Th-17 inflammatory response at the injury site

Burns. 2011 Jun;37(4):646-51. doi: 10.1016/j.burns.2011.01.028. Epub 2011 Feb 24.

Abstract

Introduction: The high incidence of morbidity and mortality following major burn can be in part attributed to immune dysfunction and wound healing complications. Inflammation plays a major role in the complex process of wound repair. Recently, a novel class of T-helper cells, termed Th-17 cells, has been found to secrete the pro-inflammatory cytokines IL-17 and IL-22. The Th-17 response also involves other cytokines, such as IL-6 and TGF-β, which have been shown to be associated with burn-induced inflammation. Nonetheless, the relationships between the Th-17 response and post-burn inflammation are unknown.

Methods: C57BL/6 male mice (n = 5-6/group) were subjected to a major burn (25% TBSA) or sham procedure. Three hours thereafter, skin samples were collected (uninjured skin and burn skin) and processed for the determination of Th-17 cytokine (IL-6, IL-17, IL-22, IL-23, IL-27, and TGF-β) levels by ELISA.

Results: At 3h after burn a significant (~3-fold) increase in tissue levels of IL-17 and IL-22 was observed at the burn site as compared to sham skin. The burn-induced Th-17 response was independent of statistically significant changes in other Th-17 cytokines (i.e., IL-6, IL-23, IL-27 and TGF-β).

Conclusions: These findings indicate the development of a robust Th-17 response at the burn site that may play an important role in subsequent immune and wound healing derangements.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Burns / immunology*
  • Burns / pathology
  • Cytokines / metabolism*
  • Enzyme-Linked Immunosorbent Assay
  • Interleukin-17 / immunology*
  • Interleukins / metabolism
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Th17 Cells / immunology*
  • Transforming Growth Factor beta / metabolism

Substances

  • Cytokines
  • Interleukin-17
  • Interleukins
  • Transforming Growth Factor beta