Yamamoto H, Siltharm S, deSerres S, Hultman C S, Meyer A A
Department of Surgery, University of North Carolina School of Medicine, Chapel Hill 27599-7210, USA.
J Trauma. 1996 Oct;41(4):612-9; discussion 620-1. doi: 10.1097/00005373-199610000-00004.
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 burn 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 for 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 not 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.
研究了前列腺素E2（PGE2）在烧伤后抑制B细胞功能中的作用。在烧伤后8天从小鼠分离烧伤或假烧伤后的脾细胞，在添加或不添加前列腺素E2（PGE2）或吲哚美辛（Indo）的情况下，与脂多糖一起培养。测定培养上清液中抗肽聚糖多糖免疫球蛋白（Ig）M（细菌抗原特异性抗体）、总IgM和总IgG水平以及淋巴细胞增殖情况。烧伤损伤显著抑制所有B细胞功能。PGE2抑制除IgG合成外的所有B细胞功能。Indo使抗肽聚糖多糖IgM恢复到正常水平，但对抑制的增殖和总IgM合成没有显著影响。PGE2增加IgG合成，Indo抑制IgG合成。虽然并非所有B细胞抑制都由PGE2引起，但这种前列腺素似乎是抗原特异性抗体反应受损和同种型转换的一个机制。成功恢复对细菌抗原的特异性抗体合成表明环氧化酶阻断剂在烧伤后具有潜在治疗作用。
