Limper A H
Department of Biochemistry and Molecular Biology, Mayo Clinic and Foundation, Rochester, MN 55905, USA.
Semin Respir Infect. 1998 Dec;13(4):339-47.
Pneumocystis carinii continues to represent an important complication of immunosuppression in patients with acquired immune deficiency syndrome, hematological and solid malignancies, organ transplantation, and during corticosteroid and cytotoxic therapy for inflammatory disorders. Although host defenses against this organism center around CD4 lymphocytic function, additional immune mediators in the alveolar spaces contribute substantially to host recognition and elimination of P. carinii. In particular, this review considers the interactions of P. carinii with alveolar macrophages, adhesive glycoproteins including vitronectin and fibronectin, and surfactant lipids and protein components. Recent studies indicate that alveolar macrophages contribute significantly to host responses against this organism by mediating uptake and degradation of P. carinii, and by releasing inflammatory mediators including reactive oxidants, eicosanoids, and the potent proinflammatory cytokine tumor necrosis factor-alpha. Furthermore, the interactions of P. carinii with multiple adhesive proteins and with surfactant components additionally modulate the interactions of P. carinii with macrophages and enhance host recognition of this pathogen. These non-lymphocytic mediators represent additional important mechanisms of host recognition and response to P. carinii infection.
卡氏肺孢子菌仍然是获得性免疫缺陷综合征、血液系统及实体恶性肿瘤、器官移植患者，以及在接受皮质类固醇和细胞毒性药物治疗炎症性疾病期间免疫抑制的一种重要并发症。尽管宿主针对这种病原体的防御主要围绕CD4淋巴细胞功能，但肺泡腔内的其他免疫介质在很大程度上有助于宿主识别和清除卡氏肺孢子菌。特别是，本综述探讨了卡氏肺孢子菌与肺泡巨噬细胞、包括玻连蛋白和纤连蛋白在内的黏附糖蛋白，以及表面活性物质脂质和蛋白质成分之间的相互作用。最近的研究表明，肺泡巨噬细胞通过介导卡氏肺孢子菌的摄取和降解，并释放包括活性氧化剂、类花生酸和强效促炎细胞因子肿瘤坏死因子-α在内的炎症介质，对宿主针对这种病原体的反应有显著贡献。此外，卡氏肺孢子菌与多种黏附蛋白以及表面活性物质成分的相互作用还可调节卡氏肺孢子菌与巨噬细胞的相互作用，并增强宿主对这种病原体的识别。这些非淋巴细胞介质代表了宿主识别和应对卡氏肺孢子菌感染的其他重要机制。
