Szabo G, Kodys K, Miller-Graziano C L
Department of Surgery, University of Massachusetts Medical Center, Worcester 01655.
J Clin Immunol. 1991 Nov;11(6):326-35. doi: 10.1007/BF00918798.
This study demonstrates that immunodepressed trauma patients' monocytes produce elevated interleukin-6 to adherence, bacterial, and cytokine stimulation compared to immunocompetent trauma patients' or normals' monocytes, suggesting their in vivo preactivation possibly mediated by the hyperimmunoglobulinemia which characterizes these patients. Furthermore, stimulation of monocytes through cross-linking their Fc gamma RI induces and augments interleukin-6 (IL-6) production to subsequent stimulation both in trauma patients' (P less than 0.001) and in normals' (P less than 0.001) monocytes. As we reported earlier, immunodepressed trauma patients have an increased proportion of Fc gamma RI-bearing monocytes in their total monocyte population and here we show that those Fc gamma RI+ monocytes produce significantly elevated interleukin-6, suggesting a relationship between elevated monocyte interleukin-6 production and Fc gamma RI triggering. Interleukin-6 induction by FcRI stimulation is not mediated solely by FcRI-induced M phi tumor necrosis factor alpha, IL-1 alpha, or IL-1 beta production and is independent of M phi prostaglandin E2 levels. Therefore, FcRI stimulation-induced elevated M phi IL-6 might contribute to the increased immunoglobulin levels posttrauma.
本研究表明,与免疫功能正常的创伤患者或正常人的单核细胞相比,免疫抑制的创伤患者的单核细胞在受到黏附、细菌和细胞因子刺激时会产生更高水平的白细胞介素-6,这表明其体内的预激活可能由这些患者所特有的高免疫球蛋白血症介导。此外,通过交联创伤患者(P<0.001)和正常人(P<0.001)单核细胞的FcγRI来刺激单核细胞,会诱导并增强其对后续刺激产生白细胞介素-6(IL-6)的能力。正如我们之前所报道的,免疫抑制的创伤患者在其单核细胞总数中,携带FcγRI的单核细胞比例增加,并且我们在此表明,那些FcγRI+单核细胞产生的白细胞介素-6显著升高,这表明单核细胞白细胞介素-6产生增加与FcγRI触发之间存在关联。FcRI刺激诱导的白细胞介素-6并非仅由FcRI诱导的巨噬细胞肿瘤坏死因子α、IL-1α或IL-1β产生所介导,并且与巨噬细胞前列腺素E2水平无关。因此,FcRI刺激诱导的巨噬细胞IL-6升高可能导致创伤后免疫球蛋白水平增加。