title: Burn-induced alterations in toll-like receptor-mediated responses by bronchoalveolar lavage cells.
abstract: Burn is associated with profound inflammation and activation of the innate immune system in multiple organ beds, including the lung. Similarly, toll-like receptors (TLR) are associated with innate immune activation. Nonetheless, it is unclear what impact burn has on TLR-induced inflammatory responses in the lung.
  
  
  METHODS
  Male C57BL/6 mice were subjected to burn (3rd degree, 25% TBSA) or sham procedure and 1, 3 or 7 days thereafter, bronchoalveolar lavage (BAL) fluid was collected and cells were isolated and cultured in vitro with specific TLR agonists as follows: Zymosan (TLR-2), LPS (TLR-4) and CpG-ODN (TLR-9). Supernatants were collected 48 h later and assayed for inflammatory cytokine levels (IL-1β, IL-6, IL-10, IL-17, TNF-α, KC, MCP-1, MIP-1α, MIP-1β and RANTES) by Bioplex.
  
  
  RESULTS
  BAL fluid from sham and burn mice did not contain detectable cytokine levels. BAL cells, irrespective of injury, were responsive to TLR-2 and TLR-4 activation. Seven days after burn, TLR-2 and TLR-4 mediated responses by BAL cells were enhanced as evidenced by increased production of IL-6, IL-17, TNF-α, MCP-1, MIP-1β and RANTES.
  
  
  CONCLUSIONS
  Burn-induced changes in TLR-2 and TLR-4 reactivity may contribute to the development of post-burn complications, such as acute lung injury (ALI) and adult respiratory distress syndrome (ARDS).
authors.affiliation: Department of Surgery, The University of Texas Health Science Center, San Antonio, TX 78229, USA. oppeltz@uthscsa.edu
authors.forename: Richard F
authors.initials: RF
authors.lastname: Oppeltz
authors.forename: Meenakshi
authors.initials: M
authors.lastname: Rani
authors.forename: Qiong
authors.initials: Q
authors.lastname: Zhang
authors.forename: Martin G
authors.initials: MG
authors.lastname: Schwacha
mesh_terms: D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology*; D002056:Burns / Q000276:immunology*; D002478:Cells, Cultured; D003470:Culture Media / Q000032:analysis; D016207:Cytokines / Q000032:analysis / Q000096:biosynthesis; D007113:Immunity, Innate; D008070:Lipopolysaccharides / Q000494:pharmacology; D008168:Lung / Q000276:immunology*; D008264:Macrophages / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009838:Oligodeoxyribonucleotides / Q000494:pharmacology; D051195:Toll-Like Receptor 2 / Q000276:immunology* / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000276:immunology* / Q000378:metabolism; D051193:Toll-Like Receptors / Q000819:agonists / Q000276:immunology*; D015054:Zymosan / Q000494:pharmacology
chemical_list: C408982:CPG-oligonucleotide; D003470:Culture Media; D016207:Cytokines; D008070:Lipopolysaccharides; D009838:Oligodeoxyribonucleotides; C493486:Tlr2 protein, mouse; C493487:Tlr4 protein, mouse; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors; D015054:Zymosan