LeVine A M, Whitsett J A, Gwozdz J A, Richardson T R, Fisher J H, Burhans M S, Korfhagen T R
Children's Hospital Medical Center, Division of Pulmonary Biology and Critical Care Medicine, Cincinnati, OH 45229, USA.
J Immunol. 2000 Oct 1;165(7):3934-40. doi: 10.4049/jimmunol.165.7.3934.
Mice lacking surfactant protein (SP)-A (SP-A-/-) or SP-D (SP-D-/-) and wild-type mice were infected with group B streptococcus or Haemophilus influenzae by intratracheal instillation. Although decreased killing of group B streptococcus and H. influenzae was observed in SP-A-/- mice but not in SP-D-/- mice, deficiency of either SP-A or SP-D was associated with increased inflammation and inflammatory cell recruitment in the lung after infection. Deficient uptake of bacteria by alveolar macrophages was observed in both SP-A- and SP-D-deficient mice. Isolated alveolar macrophages from SP-A-/- mice generated significantly less, whereas those from SP-D-/- mice generated significantly greater superoxide and hydrogen peroxide compared with wild-type alveolar macrophages. In SP-D-/- mice, bacterial killing was associated with increased lung inflammation, increased oxidant production, and decreased macrophage phagocytosis. In contrast, in the absence of SP-A, bacterial killing was decreased and associated with increased lung inflammation, decreased oxidant production, and decreased macrophage phagocytosis. Increased oxidant production likely contributes to effective bacterial killing in the lungs of SP-D-/- mice. The collectins, SP-A and SP-D, play distinct roles during bacterial infection of the lung.
通过气管内滴注，将缺乏表面活性蛋白（SP）-A（SP-A-/-）或SP-D（SP-D-/-）的小鼠以及野生型小鼠感染B族链球菌或流感嗜血杆菌。虽然在SP-A-/-小鼠中观察到对B族链球菌和流感嗜血杆菌的杀伤作用降低，但在SP-D-/-小鼠中未观察到这种情况，不过感染后，SP-A或SP-D的缺乏均与肺部炎症增加和炎症细胞募集有关。在SP-A和SP-D缺陷型小鼠中均观察到肺泡巨噬细胞对细菌的摄取不足。与野生型肺泡巨噬细胞相比，来自SP-A-/-小鼠的分离肺泡巨噬细胞产生的超氧化物和过氧化氢明显更少，而来自SP-D-/-小鼠的则明显更多。在SP-D-/-小鼠中，细菌杀伤与肺部炎症增加、氧化剂产生增加以及巨噬细胞吞噬作用降低有关。相反，在缺乏SP-A的情况下，细菌杀伤减少，并与肺部炎症增加、氧化剂产生减少以及巨噬细胞吞噬作用降低有关。氧化剂产生增加可能有助于SP-D-/-小鼠肺部有效杀灭细菌。凝集素SP-A和SP-D在肺部细菌感染过程中发挥不同作用。
