Gideoni O, Naot Y
Ann Microbiol (Paris). 1984 Jan-Feb;135A(1):55-62. doi: 10.1016/s0769-2609(84)80059-9.
The effects of interactions between mouse lymphocytes, peritoneal macrophages and Mycoplasma pulmonis mitogens on the growth of infective M. pulmonis in infected cultures were studied. Lymphocytes transformed into blast cells following in vitro exposure to either M. pulmonis mitogens or concanavalin A supported the multiplication of M. pulmonis to a greater extent than did unsensitized lymphocytes. Mitogenic stimulation of lymphocytes by M. pulmonis did not induce the release in vitro of lymphokines capable of enhancing the killing of infective organisms by mouse peritoneal macrophages. In addition, it has been shown that direct interactions of sensitized lymphocytes with macrophages in the presence of M. pulmonis mitogens not only did not enhance phagocytosis of the infecting organisms, but rather provided improved culture conditions for the replication of M. pulmonis as compared to cultures of macrophages with unsensitized lymphocytes or macrophages cultured alone. It can therefore be concluded that mycoplasmastatic or mycoplasmacidic capacities of mouse peritoneal macrophages are not enhanced due to the interactions of macrophages with lymphocytes sensitized by M. pulmonis mitogens.
研究了小鼠淋巴细胞、腹腔巨噬细胞与肺支原体促细胞分裂原之间的相互作用对感染培养物中感染性肺支原体生长的影响。体外暴露于肺支原体促细胞分裂原或伴刀豆球蛋白A后转化为母细胞的淋巴细胞比未致敏淋巴细胞更能支持肺支原体的增殖。肺支原体对淋巴细胞的促有丝分裂刺激并未在体外诱导能够增强小鼠腹腔巨噬细胞对感染性生物体杀伤作用的淋巴因子释放。此外,研究表明,在肺支原体促细胞分裂原存在的情况下,致敏淋巴细胞与巨噬细胞的直接相互作用不仅没有增强感染性生物体的吞噬作用,而且与巨噬细胞与未致敏淋巴细胞共培养或单独培养巨噬细胞相比,为肺支原体的复制提供了更好的培养条件。因此可以得出结论,小鼠腹腔巨噬细胞的支原体抑制或杀支原体能力不会因巨噬细胞与经肺支原体促细胞分裂原致敏的淋巴细胞相互作用而增强。