Cundell D R, Gerard C, Idanpaan-Heikkila I, Tuomanen E I, Gerard N P
Laboratory of Molecular Infectious Diseases, Rockefeller University, New York, New York, USA.
Adv Exp Med Biol. 1996;416:89-94. doi: 10.1007/978-1-4899-0179-8_16.
Streptococcus pneumoniae can produce asymptomatic colonization or aggressive sepsis. We sought to differentiate the molecular mechanisms of these disparate courses. Cytokine or thrombin activation of human vascular endothelial cells and type II pneumocytes enhanced pneumococcal adherence relative to resting cells. Adherence and subsequent invasion was dramatically reduced by PAF receptor antagonists. Cells transfected with the PAF receptor gained the ability to support pneumococcal adherence. PAF or PAF receptor antagonists inhibited attachment and invasion. Adherence involved phosphorylcholine on the pneumococcal teichoic acid. Virulent pneumococci target the PAF receptor on activated human cells, a necessary step to facilitate subsequent invasion.
肺炎链球菌可引起无症状定植或侵袭性败血症。我们试图区分这些不同病程的分子机制。相对于静息细胞，人血管内皮细胞和II型肺细胞的细胞因子或凝血酶激活增强了肺炎球菌的黏附。PAF受体拮抗剂可显著降低黏附和随后的侵袭。转染了PAF受体的细胞获得了支持肺炎球菌黏附的能力。PAF或PAF受体拮抗剂抑制黏附和侵袭。黏附涉及肺炎球菌磷壁酸上的磷酸胆碱。有毒力的肺炎球菌靶向活化人细胞上的PAF受体，这是促进随后侵袭的必要步骤。
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