title: Thalidomide decreases the plasma levels of IL-1 and TNF following burn injury: is it a new drug for modulation of systemic inflammatory response.
abstract: TNF and IL-1, which are produced from phagocytic cells, can produce a significant systemic inflammatory response independently by inducing systemic leukocyte and endothelial cell activation. These cytokines play a pivotal role in development of systemic inflammatory response after severe burn. Thalidomide has been shown to decrease the secretion of TNF from phagocytic cells, therefore suppression of TNF and IL-1 production from activated phagocytic cells might be a successful treatment modality for prevention of systemic inflammatory response following severe burn. To address this issue, we aimed to show whether thalidomide treatment decreased or suppressed plasma levels of TNF and IL-1 following burn in rats. Following the injury, 36 rats were randomly separated into two experimental groups at the third and seventh days. Rats in the experimental group had oral thalidomide (10mg/kg day) treatment for three and seven consecutive days whereas animals in control groups had no treatment. Thalidomide treatment decreased TNF and IL-1 significantly in both experimental groups at both the points (P<0.05). Although in this study we just showed inhibitory effect of thalidomide on plasma the level of TNF and IL-1, we speculate that thalidomide may have modulatory effect on the systemic inflammatory response after burn by decreasing plasma levels of TNF and IL-1.
authors.affiliation: Department of Plastic and Reconstructive Surgery and Burn Center, Gulhane Military Medical Academy and Medical School, 06018 Etlik, Ankara, Turkey. muhieski@yahoo.com
authors.forename: Muhitdin
authors.initials: M
authors.lastname: Eski
authors.forename: Ismail
authors.initials: I
authors.lastname: Sahin
authors.forename: Mustafa
authors.initials: M
authors.lastname: Sengezer
authors.forename: Muhittin
authors.initials: M
authors.lastname: Serdar
authors.forename: Ahmet
authors.initials: A
authors.lastname: Ifran
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology / Q000627:therapeutic use; D002056:Burns / Q000097:blood* / Q000150:complications; D004353:Drug Evaluation, Preclinical; D007375:Interleukin-1 / Q000097:blood*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood* / Q000209:etiology / Q000517:prevention & control; D013792:Thalidomide / Q000494:pharmacology* / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D013792:Thalidomide