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

Hiromasa Yamamoto, Soranit Siltharm, Suzan DeSerres, C. Scott Hultman, Anthony A. Meyer

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)612-621
Number of pages10
JournalJournal of Trauma - Injury, Infection and Critical Care
Issue number4
StatePublished - Oct 1996
Externally publishedYes


  • B-cell
  • Bacterial infection
  • Burn injury
  • Indomethacin
  • Prostaglandin E

ASJC Scopus subject areas

  • Surgery
  • Critical Care and Intensive Care Medicine


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