Morikawa K, Watabe H, Araake M, Morikawa S
Department of Internal Medicine, Shimane Medical University, Japan.
Antimicrob Agents Chemother. 1996 Jun;40(6):1366-70. doi: 10.1128/AAC.40.6.1366.
Some antimicrobial agents have been reported to modify the host immune and inflammatory responses both in vivo and in vitro. Fosfomycin (FOM) and clarithromycin (CAM) have immunomodulatory activity on human lymphocyte function. In the present study, we examined the effects of FOM and CAM on cytokine synthesis by lipopolysaccharide (LPS)-stimulated human monocytes in comparison with that of dexamethasone in vitro. The three drugs demonstrated positive or negative effects on the synthesis of various cytokines by LPS-primed monocytes. They suppressed the synthesis of tumor necrosis factor alpha, interleukin 1 alpha (IL-1 alpha), IL-1 beta, the IL-1 receptor antagonist, and granulocyte-macrophage colony-stimulating factor in a concentration-dependent manner at concentrations between 1.6 and 40 micrograms/ml. On the contrary, the drugs showed different actions on the synthesis of IL-6 and IL-10. Namely, FOM enhanced both IL-6 and IL-10 synthesis, CAM enhanced only IL-10 synthesis, but dexamethasone deeply suppressed the synthesis of both cytokines. These data indicate that antibacterial agents may modify acute-phase inflammatory responses through their effects on cytokine synthesis by monocytes.
据报道,一些抗菌药物在体内和体外均可改变宿主的免疫和炎症反应。磷霉素(FOM)和克拉霉素(CAM)对人淋巴细胞功能具有免疫调节活性。在本研究中,我们在体外比较了FOM和CAM与地塞米松对脂多糖(LPS)刺激的人单核细胞合成细胞因子的影响。这三种药物对LPS预处理的单核细胞合成各种细胞因子表现出阳性或阴性作用。它们在1.6至40微克/毫升的浓度范围内以浓度依赖性方式抑制肿瘤坏死因子α、白细胞介素1α(IL-1α)、IL-1β、IL-1受体拮抗剂和粒细胞-巨噬细胞集落刺激因子的合成。相反,这些药物对IL-6和IL-10的合成表现出不同的作用。具体而言,FOM增强IL-6和IL-10的合成,CAM仅增强IL-10的合成,但地塞米松则深度抑制这两种细胞因子的合成。这些数据表明,抗菌药物可能通过影响单核细胞合成细胞因子来改变急性期炎症反应。