Morikawa K, Oseko F, Morikawa S
Department of Internal Medicine, Shimane Medical University, Japan.
Antimicrob Agents Chemother. 1993 Feb;37(2):270-5. doi: 10.1128/AAC.37.2.270.
Fosfomycin (FOM) is an unique antibiotic which is chemically unrelated to any other known antimicrobial agent. Recent investigations have demonstrated that FOM inhibits histamine release from basophils. In this study, we examined the effect of FOM on human B-cell functions. FOM inhibited the proliferative response of resting B cells induced by Staphylococcus aureus Cowan 1 in a dose-dependent manner. FOM interfered with the transition from the G0 to the G1 phase of the cell cycle, leading to cell arrest. The proliferative response of in vivo-activated B cells and lymphokine-induced B-cell proliferation were also affected by FOM. In addition, FOM suppressed immunoglobulin secretion by antibody-producing B cells. Interestingly, FOM did not affect the expression of activation antigens such as the CD25 (interleukin-2 receptor) and CD71 (transferrin receptor) antigens. Moreover, FOM sustained the increased Ia expression on B-cell membranes induced by S. aureus Cowan 1 stimulation, which suggests that FOM may not block the role of B cells in antigen presentation in T-cell-B-cell interaction.
磷霉素（FOM）是一种独特的抗生素，其化学结构与其他任何已知抗菌剂均无关联。最近的研究表明，FOM可抑制嗜碱性粒细胞释放组胺。在本研究中，我们检测了FOM对人B细胞功能的影响。FOM以剂量依赖的方式抑制了金黄色葡萄球菌Cowan 1诱导的静息B细胞的增殖反应。FOM干扰了细胞周期从G0期到G1期的转变，导致细胞停滞。体内活化B细胞的增殖反应以及淋巴因子诱导的B细胞增殖也受到FOM的影响。此外，FOM抑制了产生抗体的B细胞分泌免疫球蛋白。有趣的是，FOM不影响诸如CD25（白细胞介素-2受体）和CD71（转铁蛋白受体）等活化抗原的表达。而且，FOM维持了金黄色葡萄球菌Cowan 1刺激诱导的B细胞膜上Ia表达的增加，这表明FOM可能不会在T细胞-B细胞相互作用中阻断B细胞在抗原呈递中的作用。
