Downregulation of immune signaling genes in patients with large surface burn injury.
We sought to evaluate the temporal pattern of expression of important immune signaling genes in patients with varied TBSA burn injury during the first week after burn. Peripheral blood mononuclear cell fractions were collected from each patient (N = 10) at two time points, one immediately following burn injury, and the other 1 week later. The change in gene expression was correlated with all clinical data including burn size. It was found that gene expression was indirectly proportional with burn size. Smaller burns (<30%) TBSA resulted in an up-regulation of several genes measured, while larger burns (>30%) TBSA resulted in significant down-regulation. In conclusion, a larger burn establishes conditions for severe immunosuppression by down-regulating key immune signaling genes and could be one explanation for the increased susceptibility of major burns to infection. These data shed light on the etiology of burn-induced immune dysfunction in humans and support a more comprehensive genomic profile study in burn patients.
Moore
Chris B
CB
Department of Microbiology-Immunology, Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, North Carolina 27599-7228, USA.
Medina
Miguel A
MA
van Deventer
Hendrik W
HW
O'Connor
Brian P
BP
Cameron
Scott
S
Taxman
Debra J
DJ
Maile
Robert
R
Ting
Jenny P-Y
JP
Cairns
Bruce A
BA
D000293:Adolescent; D000328:Adult; D000368:Aged; D002056:Burns / Q000378:metabolism* / Q000473:pathology; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D003428:Cross Infection / Q000382:microbiology; D015536:Down-Regulation; D005260:Female; D020869:Gene Expression Profiling; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D053592:Interleukin-1 Receptor-Associated Kinases / Q000235:genetics / Q000378:metabolism; D018664:Interleukin-12 / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics / Q000378:metabolism; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D053474:Nod1 Signaling Adaptor Protein / Q000235:genetics / Q000378:metabolism; D053473:Nod2 Signaling Adaptor Protein / Q000235:genetics / Q000378:metabolism; D009894:Opportunistic Infections / Q000382:microbiology; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism; D048029:TNF Receptor-Associated Factor 6 / Q000235:genetics / Q000378:metabolism; D051193:Toll-Like Receptors / Q000235:genetics / Q000378:metabolism
D002352:Carrier Proteins; D036341:Intercellular Signaling Peptides and Proteins; D015850:Interleukin-6; C507779:MYD88 protein, human; D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C503285:NLRC3 protein, human; C453881:NLRP3 protein, human; C119067:NOD1 protein, human; C429018:NOD2 protein, human; D053474:Nod1 Signaling Adaptor Protein; D053473:Nod2 Signaling Adaptor Protein; D012333:RNA, Messenger; D048029:TNF Receptor-Associated Factor 6; D051193:Toll-Like Receptors; D018664:Interleukin-12; D053592:Interleukin-1 Receptor-Associated Kinases