title: The effect of burn injury on suppressors of cytokine signalling.
abstract: The newly identified suppressors of cytokine signaling (SOCS) family of proteins act as intracellular inhibitors of several cytokine signal transduction pathways. Their expression is induced by cytokine activation of the Janus kinase/signal transducer and activator of transcription (Jak/STAT) pathway, and they act as a negative feedback loop by subsequently inhibiting the Jak/STAT pathway either by direct interaction with activated Jaks or with the receptors. In this study we investigated the expression and translation of SOCS proteins after burn injury. Thermal injury increased the expression of SOCS3 compared with sham at 4 h, 24 h, and 10 days after thermal injury in the liver. SOCS3 protein was increased at 4 and 24 h after thermal injury in the liver. Expression of SOCS1 mRNA was not detected in sham or burn liver. SOCS2 mRNA and cytokine-inducible SH2-containing protein (CIS) mRNA were detected at the same levels for both sham and burn at all time points in the liver. In the spleen there was a trend towards an increase in SOCS1 mRNA at all time points; thermal injury significantly decreased SOCS2 mRNA compared with sham at 4 h, SOCS3 mRNA was significantly increased at 24 h compared with 10 days, and CIS mRNA was detected at the same levels for both sham and burn at all time points. In conclusion, thermal injury causes elevations in SOCS3 within 4 h after a burn, reaching a maximum at 24 h post injury. Levels continue to be elevated for up to 10 days post injury. SOCS3 may be very important in regulating the balance between immunosuppression and inflammation after thermal injury.
authors.affiliation: Shriners Hospital for Children, Cincinnati, Ohio 45229, USA.
authors.forename: C K
authors.initials: CK
authors.lastname: Ogle
authors.forename: F
authors.initials: F
authors.lastname: Kong
authors.forename: X
authors.initials: X
authors.lastname: Guo
authors.forename: D A
authors.initials: DA
authors.lastname: Wells
authors.forename: S
authors.initials: S
authors.lastname: Aosasa
authors.forename: G
authors.initials: G
authors.lastname: Noel
authors.forename: N
authors.initials: N
authors.lastname: Horseman
mesh_terms: D000818:Animals; D002056:Burns / Q000276:immunology* / Q000378:metabolism; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism*; D004268:DNA-Binding Proteins; D005786:Gene Expression Regulation; D017874:Immediate-Early Proteins / Q000235:genetics / Q000378:metabolism; D007375:Interleukin-1 / Q000235:genetics; D016753:Interleukin-10 / Q000235:genetics; D015850:Interleukin-6 / Q000235:genetics; D008070:Lipopolysaccharides; D008099:Liver / Q000276:immunology / Q000378:metabolism*; D008297:Male; D011506:Proteins / Q000235:genetics / Q000378:metabolism; D051381:Rats; D011912:Rats, Inbred ACI; D012097:Repressor Proteins; D015398:Signal Transduction; D013154:Spleen / Q000276:immunology / Q000378:metabolism; D000071222:Suppressor of Cytokine Signaling 1 Protein; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D015534:Trans-Activators; D014157:Transcription Factors
chemical_list: D002352:Carrier Proteins; D016207:Cytokines; D004268:DNA-Binding Proteins; D017874:Immediate-Early Proteins; D007375:Interleukin-1; D016753:Interleukin-10; D015850:Interleukin-6; D008070:Lipopolysaccharides; D011506:Proteins; D012097:Repressor Proteins; D000071222:Suppressor of Cytokine Signaling 1 Protein; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D015534:Trans-Activators; D014157:Transcription Factors; C491589:Socs1 protein, rat; C491408:Socs2 protein, rat; C491410:Socs3 protein, rat