Effect of cyclo-oxygenase inhibition on in vitro B-cell function after burn injury

The role of PGE₂ in suppression of B-cell function after burn injury was investigated. Splenocytes from burned or sham-burned mice were isolated 8 days after born injury and cultured with lipopolysaccharide with or without the addition of prostaglandin E₂ (PGE₂) or indomethacin (Indo). Anti- peptidoglycan polysaccharide immunoglobulin (Ig)M (specific antibody to a bacterial antigen), total IgM, and total IgG levels in culture supernatant and lymphocyte proliferation were measured. All B-cell functions were significantly suppressed by burn injury. PGE₂ suppressed all B-cell functions except fur IgG synthesis. Indo restored anti-peptidoglycan polysaccharide IgM to normal levels, but did not have a significant effect on suppressed proliferation and total IgM synthesis. IgG synthesis was increased by PGE₂ and inhibited by Indo. Although nut all B-cell suppression was accounted for by PGE₂, this prostaglandin appeared to be a mechanism responsible for impaired antigen specific antibody response and isotype switching. Successful restoration of specific antibody synthesis to bacterial antigen suggests a potential therapeutic role for a cyclo-oxygenase blocking agent after burn injury.