EFFECT OF CYCLOOXYGENASE INHIBITION ON IN-VITRO B-CELL FUNCTION AFTERBURN INJURY

The role of PGE(2) in suppression of B-cell function after burn injury was investigated. Splenocytes from burned or sham-burned mice were is olated 8 days after burn injury and cultured with lipopolysaccharide w ith or without the addition of prostaglandin E(2) (PGE(2)) or indometh acin (Indo). Anti-peptidoglycan polysaccharide immunoglobulin (Ig)M (s pecific antibody to bacterial antigen), total IgM, and total IgG level s in culture supernatant and lymphocyte proliferation were measured. A ll B-cell functions were significantly suppressed by burn injury. PGE( 2) suppressed all B-cell functions except for IgG synthesis. Indo rest ored anti-peptidoglycan polysaccharide IgM to normal levels, but did n ot have a significant effect on suppressed proliferation and total IgM synthesis. IgG synthesis was increased by PGE(2) and inhibited by Ind o. Although not all B-cell suppression was accounted for by PGE(2), th is prostaglandin appeared to be a mechanism responsible for impaired a ntigen specific antibody response and isotype switching. Successful re storation of specific antibody synthesis to bacterial antigen suggests a potential therapeutic role for a cycle-oxygenase blocking agent aft er burn injury.