Cyclooxygenase 2-mediated suppression of macrophage interleukin-12 production after thermal injury.
Cyclooxygenase 2-mediated suppression of macrophage interleukin-12 production after thermal injury.
复制标题
热损伤后环加氧酶 2 介导的巨噬细胞白细胞介素 12 产生抑制。
DOI：
10.1152/ajpcell.00357.2001
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Chaudry,IrshadH
中科院分区：
文献类型：
--
作者：
Schwacha,MartinG;Chung,Chun-Shiang;Ayala,Alfred;Bland,KirbyI;Chaudry,IrshadH
Macrophage (Mφ) prostaglandin (PG)E2production has been implicated in immunosuppression and increased susceptibility to sepsis after thermal injury. Deficient interleukin (IL)-12 production has also been implicated in these postburn complications. The present study examined the relationship between Mφ cyclooxygenase (COX)-2 activity and IL-12 production after thermal injury. C57BL/6 female mice were subjected to a 25% total body surface area full-thickness burn. Mφ were isolated 7 days later, or the mice were subjected to sepsis by cecal ligation and puncture (CLP). IL-12 production by Mφ from injured mice was suppressed by >50%, whereas COX-2 expression and PGE2production were increased twofold. The COX-2 inhibitor NS-398 suppressed PGE2production and normalized IL-12 production in the injury group, whereas it had no effect on IL-10 production. Injured mice subjected to CLP had lower IL-12 plasma levels compared with sham-treated mice subjected to CLP. NS-398 treatment prevented the suppression in plasma IL-12 levels in the injury group. Thus elevated Mφ COX-2 activity, independent of IL-10, suppresses Mφ IL-12 production after thermal injury and may play an important role in the observed immunosuppression under such conditions.
