Prostaglandin E2 depresses antigen-presenting cell function of peritoneal macrophages.
Prostaglandin E2 depresses antigen-presenting cell function of peritoneal macrophages.
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前列腺素 E2 抑制腹膜巨噬细胞的抗原呈递细胞功能。
DOI：
10.1016/0022-4804(88)90108-4
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Chaudry,IH
中科院分区：
文献类型：
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作者：
Stephan,RN;Conrad,PJ;Saizawa,M;Dean,RE;Chaudry,IH
类花生酸在创伤中起着重要作用。这种炎症介质对细胞介导的免疫（CMI）产生负面影响。然而，没有关于类花生酸对CMI中关键事件的影响的信息，即，巨噬细胞（Mφ）的抗原呈递（AP）细胞功能，这是一种负责T和B淋巴细胞活化的细胞过程。本研究旨在探讨前列腺素E_2（PGE_2）和血栓素B_2（TXB_2）对腹腔Mφ AP细胞功能的影响。为了研究这一点，使用了T辅助细胞克隆D10.G4.1。该细胞克隆在携带Mφ和特异性抗原（伴白蛋白A）的Iak（II类糖蛋白，MAC产物）存在下增殖，从而直接反映了Mφ的AP能力。取B10.BR小鼠（H2k）腹腔Mφ，用不同浓度的PGE_2或TXB_2与2 × 104 D_（10.G4.1）细胞/孔和伴白蛋白（400 μg/ml）共同孵育。将培养物孵育72小时，用[3 H]-胸苷脉冲，并收获。在10、30和100 nM的PGE 2浓度下，D10.G4.1增殖分别为对照的38、35和20%（与对照相比P< 0.05）。上述浓度的TXB 2对D10的增殖反应无抑制作用。因此，PGE 2对腹腔Mφ AP有较强的免疫抑制作用，而TXB 2对AP无明显抑制作用。上述结果提示，出血和创伤时PGE 2水平升高可能通过抑制Mφ AP细胞功能而导致CMI紊乱。此外，这种有缺陷的AP过程可能进一步增加创伤后脓毒症和多器官衰竭的易感性。
Eicosanoids play a prominent role in trauma. Such mediators of inflammation negatively influence cell-mediated immunity (CMI). There is, however, no information available on the effect of eicosanoids on a critical event in CMI, i.e., antigen-presenting (AP) cell function of macrophages (Mφ), a cellular process responsible for the activation of T and B lymphocytes. The aim of this study, therefore, was to examine the effect of prostaglandin E2(PGE2) and thromboxane B2(TXB2) on AP cell function of the peritoneal Mφ. To study this, a T-helper-cell clone, D10.G4.1 was employed. This cell clone proliferates in the presence of Iak(Class II glycoprotein, MAC product) bearing Mφ and specific antigen (conalbumin A) thus directly reflecting the AP capability of the Mφ. Peritoneal Mφ were harvested from B10.BR mice (H2k) and their AP was testedin vitroby incubating varying numbers of Mφ with 2 × 104D10.G4.1 cells/well and conalbumin (400 μg/ml) in the presence and absence of different concentrations of PGE2or TXB2. Cultures were incubated for 72 hr, pulsed with [3H]-thymidine, and harvested. At concentrations of 10, 30, and 100 nMof PGE2, D10.G4.1 proliferations were 38, 35, and 20% of control, respectively (P< 0.05 compared to control). TXB2added at the above-mentioned concentrations did not suppress the proliferative response of D10. Thus, PGE2but not TXB2has a potent immunosuppressive effect on AP of peritoneal Mφ. The above results lead us to conclude that the elevated levels of PGE2in hemorrhage and trauma could be responsible for perturbations in CMI via depression of AP cell function of the Mφ. In addition, this defective AP process might further increase the susceptibility to sepsis and multiple organ failure following trauma.