Nakano M, Toyoda H, Tanabe M J, Matsumoto T, Masuda S
Microbiol Immunol. 1980;24(10):981-94. doi: 10.1111/j.1348-0421.1980.tb02903.x.
Polyclonal plaque-forming cell (PFC) responses in murine spleen cells induced by Staphylococcus aureus and S. epidermidis were studied. Injection of Balb/c mice with S. aureus strain 248 beta H resulted in the generation of anti-trinitrophenyl (TNP) and anti-sheep red blood cell PFC in their spleens. Cultures of Balb/c mutant yielded many anti-TNP PFC. The larger the number of organisms that were added to the cultures, the better was the PFC response. Both living and killed organisms were capable of inducing the response, but an excess of living 248 beta H organisms in the cultures abrogated the response. All of the organisms (12 strains of S. aureus and 11 strains of S. epidermidis) freshly isolated from patients had the ability to induce the polyclonal PFC response in cell cultures. These organisms stimulated cultured C3H/HcJ mouse spleen cells, which were unresponsive to bacterial lipopolysaccharide (LPS). Cultured cells from the spleens of athymic mice also responded to these organisms, and the number of PFC in nu/nu cell cultures was always greater than in nu/+ cells prepared from a haired litter mate. Moreover, the responses of nu/nu spleen were lower than expected. These findings suggest that the polyclonal PFC response to staphylococci is thymus independent, but that the magnitude of the response is regulated by mature T cells. Cultures of macrophage-depleted spleen cells responded to the organisms to an extent similar to that of the control. The 248 beta H organisms were less capable of stimulating spleen cells of 2-week-old mice (i.e., early maturing B cells) than LPS. However, spleen cells from adult (7-week-old) and aged (9-month-old) mice responded well to both the organisms and LPS. Previous sensitization with the organisms in vivo did not affect any polyclonal responses of spleen cells in vitro to either the organisms or LPS. The role of staphylococcal protein A in the polyclonal PFC response to staphylococci is discussed.
研究了金黄色葡萄球菌和表皮葡萄球菌诱导的小鼠脾细胞多克隆空斑形成细胞（PFC）反应。用金黄色葡萄球菌248βH菌株注射Balb/c小鼠，可使其脾脏产生抗三硝基苯（TNP）和抗绵羊红细胞PFC。Balb/c突变体培养物产生了许多抗TNP PFC。添加到培养物中的生物体数量越多，PFC反应越好。活的和灭活的生物体都能够诱导反应，但培养物中过量的活248βH生物体消除了反应。从患者新鲜分离的所有生物体（12株金黄色葡萄球菌和11株表皮葡萄球菌）都有能力在细胞培养物中诱导多克隆PFC反应。这些生物体刺激了对细菌脂多糖（LPS）无反应的培养C3H/HcJ小鼠脾细胞。无胸腺小鼠脾脏的培养细胞也对这些生物体有反应，nu/nu细胞培养物中的PFC数量总是多于从有毛同窝小鼠制备的nu/+细胞中的PFC数量。此外，nu/nu脾脏的反应低于预期。这些发现表明，对葡萄球菌的多克隆PFC反应不依赖胸腺，但反应的强度受成熟T细胞调节。巨噬细胞耗竭的脾细胞培养物对生物体的反应程度与对照相似。248βH生物体刺激2周龄小鼠（即早期成熟B细胞）脾细胞的能力低于LPS。然而，成年（7周龄）和老年（9月龄）小鼠的脾细胞对生物体和LPS都有良好反应。体内预先用这些生物体致敏不影响脾细胞体外对这些生物体或LPS的任何多克隆反应。讨论了葡萄球菌蛋白A在对葡萄球菌的多克隆PFC反应中的作用。
