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首页> 外文期刊>Infection and immunity >In vitro inhibition of murine macrophage migration by Bordetella pertussis lymphocytosis-promoting factor.
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In vitro inhibition of murine macrophage migration by Bordetella pertussis lymphocytosis-promoting factor.

机译：百日咳博德特氏菌淋巴细胞促进因子体外抑制鼠巨噬细胞迁移。

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Lymphocytosis promoting factor (LPF) of Bordetella pertussis is a protein toxin which may have a role in the pathogenesis of pertussis. Since macrophages have an important role in the control of respiratory infections, the in vitro effects of LPF on macrophages from C3H/HeN and C3H/HeJ mice and on a murine macrophage-like cell line, RAW264, were examined. LPF inhibited random migration of resident peritoneal macrophages as well as the chemotaxis of peritoneal macrophages and the cell line. Fifty percent inhibition of chemotaxis occurred at 0.2 to 0.3 ng of LPF per ml for the macrophages and at 1 to 2 ng of LPF per ml for the cell line. When LPF was either heated at 80 degrees C for 5 min or premixed with specific antibodies, it failed to inhibit migration. At 20 ng/ml, LPF inhibited chemotaxis by more than 80% and also decreased Fc-mediated phagocytosis by 25 to 35%. At this dose, LPF was not a chemoattractant for murine macrophages and did not reduce macrophage viability, adherence, or opsonized zymosan-stimulated superoxide release. When LPF-treated macrophages were added to tissue culture dishes and then examined microscopically after 4 h, the LPF-treated cells adhered but failed to spread and elongate as well as control macrophages. These data indicate that LPF specifically inhibits macrophage migration in vitro and suggest that a possible role for LPF in pathogenesis is to inhibit migration of macrophages to the site of B. pertussis infection.
机译：百日咳博德特氏菌的淋巴细胞增生促进因子（LPF）是一种蛋白质毒素，可能在百日咳的发病机理中起作用。由于巨噬细胞在控制呼吸道感染中具有重要作用，因此研究了LPF对C3H / HeN和C3H / HeJ小鼠巨噬细胞以及鼠类巨噬细胞样细胞RAW264的体外作用。 LPF抑制常驻腹膜巨噬细胞的随机迁移以及腹膜巨噬细胞和细胞系的趋化性。对于巨噬细胞，趋化性的抑制作用发生在每毫升0.2至0.3 ng LPF和细胞系每毫升1 ng 2至2 ng LPF时。将LPF在80摄氏度下加热5分钟或与特异性抗体预混合后，无法抑制迁移。 LPF在20 ng / ml时抑制趋化性超过80％，并且将Fc介导的吞噬作用降低25％至35％。在此剂量下，LPF不是鼠巨噬细胞的化学引诱剂，并且不会降低巨噬细胞的生存力，粘附性或酵母聚糖刺激的调理素超氧化物释放。当将LPF处理的巨噬细胞添加到组织培养皿中，然后在4小时后进行显微镜检查时，LPF处理的细胞粘附但未能像对照巨噬细胞那样扩散和伸长。这些数据表明LPF体外特异性抑制巨噬细胞迁移，并暗示LPF在发病机理中的可能作用是抑制巨噬细胞迁移至百日咳博德特氏菌感染部位。

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