Damage-associated molecular patterns (DAMPs) released after burn are associated with inflammation and monocyte activation.
Burns are associated with activation of the innate immunity that can contribute to complications. Damage-associated molecular patterns (DAMPs) released after tissue injury play a critical role in the activation of the innate immunity, which appears to be mediated via toll-like receptors (TLRs). Previous findings have shown that TLRs and TLR-mediated responses are up-regulated after burn. Nonetheless, it is unclear what impact burn has on circulating levels of DAMPs. To study this, male C57BL/6 mice were subjected to a major burn or sham procedure. Three hours to 7days thereafter, plasma was collected and assayed for the representative DAMPs (i.e., HMGB1, cytochrome C, DNA and S100A) and extracellular cleavage products (fibronectin and hyaluronan). HMGB1, cytochrome C, fibronectin and hyaluronan levels were elevated in a time-dependent manner after burn as compared to sham levels. A significant elevation in TNF-α, IL-6 and IL-10 cytokine plasma levels was also found after burn. All cytokine levels were increased as early as 3h and remained elevated up to 24h. Circulating CD11b+monocytes were increased at 24h after burn and showed increased expression of TLR-2. In conclusion, these findings support the concept that burn-induced elevations in circulating DAMPs are in part responsible for monocyte activation and the development of inflammatory complications under such conditions and warrants further investigation.
Department of Surgery, The University of Texas Health Science Center at San Antonio, TX 78229, United States.
Meenakshi
M
Rani
Department of Surgery, The University of Texas Health Science Center at San Antonio, TX 78229, United States.
Susannah E
SE
Nicholson
Department of Surgery, The University of Texas Health Science Center at San Antonio, TX 78229, United States.
Qiong
Q
Zhang
Department of Surgery, The University of Texas Health Science Center at San Antonio, TX 78229, United States; US Army Institute of Surgical Research, Fort Sam Houston, TX 78234, United States. Electronic address: Schwacha@uthscsa.edu.
Martin G
MG
Schwacha
D000067531:Alarmins / Q000097:blood*; D000818:Animals; D015415:Biomarkers / Q000097:blood; D002056:Burns / Q000378:metabolism*; D045304:Cytochromes c / Q000097:blood; D004195:Disease Models, Animal; D005353:Fibronectins / Q000097:blood; D024243:HMGB1 Protein / Q000097:blood; D006820:Hyaluronic Acid / Q000097:blood; D007249:Inflammation / Q000378:metabolism*; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009000:Monocytes / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D000067531:Alarmins; D015415:Biomarkers; D005353:Fibronectins; D024243:HMGB1 Protein; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D006820:Hyaluronic Acid; D045304:Cytochromes c
Alarmins; CD11b; Danger Theory; HMGB-1; Toll-like receptors; Trauma