Jounblat R, Clark H, Eggleton P, Hawgood S, Andrew P W, Kadioglu A
MRC Immunochemistry Unit, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK.
Respir Res. 2005 Oct 28;6(1):126. doi: 10.1186/1465-9921-6-126.
We have shown previously that surfactant protein D (SP-D) binds and agglutinates Streptococcus pneumoniae in vitro. In this study, the role of SP-D in innate immunity against S. pneumoniae was investigated in vivo, by comparing the outcome of intranasal infection in surfactant protein D deficient (SP-D-/-) to wildtype mice (SP-D+/+). Deficiency of SP-D was associated with enhanced colonisation and infection of the upper and lower respiratory tract and earlier onset and longer persistence of bacteraemia. Recruitment of neutrophils to inflammatory sites in the lung was similar in both strains mice in the first 24 hrs post-infection, but different by 48 hrs. T cell influx was greatly enhanced in SP-D-/- mice as compared to SP-D+/+ mice. Our data provides evidence that SP-D has a significant role to play in the clearance of pneumococci during the early stages of infection in both pulmonary sites and blood.
我们之前已经表明,表面活性蛋白D(SP-D)在体外可结合并凝集肺炎链球菌。在本研究中,通过比较表面活性蛋白D缺陷型(SP-D-/-)小鼠与野生型小鼠(SP-D+/+)鼻内感染的结果,在体内研究了SP-D在抗肺炎链球菌天然免疫中的作用。SP-D缺陷与上、下呼吸道的定植和感染增强以及菌血症的更早发生和更长持续时间相关。在感染后最初24小时内,两品系小鼠中嗜中性粒细胞向肺部炎症部位的募集相似,但在48小时时有所不同。与SP-D+/+小鼠相比,SP-D-/-小鼠中的T细胞流入大大增强。我们的数据表明,SP-D在肺部和血液感染早期清除肺炎球菌过程中发挥着重要作用。