title: Role of mast cells in the pathogenesis of postburn inflammatory response: reactive oxygen species as mast cell stimulators.
abstract: Thermal trauma has a direct effect on mast cells, triggering the secretion of histamine. This secretion leads to an enhanced xanthine oxidase activity and an increased production of reactive oxygen species (ROS), the latter being produced after burns through differing mechanisms. As ROS have been shown to have deleterious effects on cellular membranes, a lesion of the mast cell membrane could close the circle of autoinjury due to the vasoactive actions of mast cell mediators. Our studies were designed to assess the potentiality of ROS as stimulators of mast cell degranulation after burns by comparing two groups of rats treated, respectively, with SOD and saline solution after a scald injury. Plasma levels of tryptase and histamine were analyzed as markers of mast cell activity. A comparison of the mean increases of tryptase between baseline and 3-h postburn levels in the two groups shows significant differences (p < 0.001) (control: 0.13+/-0.04, SOD: 0.03+/-0.01). When comparing the mean increases between the baseline and 3 h postburn levels of histamine in the two groups, significant differences were also found (p < 0.001) (control group: 2.70+/-0.57. SOD group: 1.22+/-0.32). The lower levels of histamine and tryptase induced by SOD provides indirect evidence that ROS are involved in the process, causing the release of such mediators by mast cells, which may in turn suggest that ROS can act as stimulators of mast cell degranulation in burns.
authors.affiliation: Experimental Surgery Unit, Hospital del Aire, Madrid, Spain. xsantos@haire.es
authors.forename: F X
authors.initials: FX
authors.lastname: Santos
authors.forename: C
authors.initials: C
authors.lastname: Arroyo
authors.forename: I
authors.initials: I
authors.lastname: García
authors.forename: R
authors.initials: R
authors.lastname: Blasco
authors.forename: J M
authors.initials: JM
authors.lastname: Obispo
authors.forename: C
authors.initials: C
authors.lastname: Hamann
authors.forename: L
authors.initials: L
authors.lastname: Espejo
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000097:blood; D002056:Burns / Q000150:complications* / Q000378:metabolism; D015550:Cell Degranulation / Q000187:drug effects / Q000502:physiology; D053818:Chymases; D004195:Disease Models, Animal; D006632:Histamine / Q000097:blood; D008297:Male; D008407:Mast Cells / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000502:physiology*; D012697:Serine Endopeptidases / Q000097:blood; D013482:Superoxide Dismutase / Q000494:pharmacology; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology* / Q000378:metabolism; D053802:Tryptases; D014969:Xanthine Oxidase / Q000097:blood
chemical_list: D015415:Biomarkers; D017382:Reactive Oxygen Species; D006632:Histamine; D013482:Superoxide Dismutase; D014969:Xanthine Oxidase; D012697:Serine Endopeptidases; C083294:chymase 2; D053818:Chymases; C509223:Tpsab1 protein, rat; C509221:Tpsb2 protein, rat; D053802:Tryptases