INTERLEUKIN-2 RECEPTOR EXPRESSION AND FUNCTION FOLLOWING THERMAL-INJURY

Citation
Ds. Oriordain et al., INTERLEUKIN-2 RECEPTOR EXPRESSION AND FUNCTION FOLLOWING THERMAL-INJURY, Archives of surgery, 130(2), 1995, pp. 165-170
Citations number
23
Categorie Soggetti
Surgery
Journal title
ISSN journal
00040010
Volume
130
Issue
2
Year of publication
1995
Pages
165 - 170
Database
ISI
SICI code
0004-0010(1995)130:2<165:IREAFF>2.0.ZU;2-1
Abstract
Background/Objective: Serious traumatic or thermal injury is associate d with depression of cellular immunity, including the failure of T-lym phocyte proliferation in response to stimulation that depends both on production of interleukin-2 (IL-2) and on expression of functional IL- 2 receptors (IL-2R). While decreased IL-2 production following thermal injury is undisputed, the status of IL-2R expression and function in this setting is controversial; therefore, we sought to investigate thi s issue. Design: A total of 20 male A/J mice (n=22 per group) were sub jected to a 20% scald burn injury or sham burn, killed 4, 7, 10, 14, o r 21 days later, and splenocytes harvested. In vitro parameters of bot h IL-2R expression and function were measured. Results: On day 7, sple nic lymphocyte proliferation and IL-2 production in response to mitoge nic stimulation were both suppressed following burn injury to 50% and 60% of controls. respectively. Northern blot analysis revealed normal IL-2R p55 messenger RNA expression in response to mitogenic stimulatio n on days 7, 10, and 14 in thermally injured animals. Phenotypic IL-2R p55 expression in concanavalin A-stimulated CD3(+) cells was unchange d following burn injury. Binding of fluorescein-labeled IL-2 to cell m embranes was increased in burned animals at days 10 and 14. The additi on of IL-2 to cultures of spleen cells from burned mice consistently r estored the mitogenic response to that of the controls. Conclusions: T hermal injury in this model does not result in either quantitative or functional suppression of IL-2R. Suppression of T-cell activation and proliferation, seen following thermal injury, appears primarily relate d to abnormal IL-2 production.