Zhang J R, Mostov K E, Lamm M E, Nanno M, Shimida S, Ohwaki M, Tuomanen E
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
Cell. 2000 Sep 15;102(6):827-37. doi: 10.1016/s0092-8674(00)00071-4.
The polymeric immunoglobulin receptor (pIgR) plays a crucial role in mucosal immunity against microbial infection by transporting polymeric immunoglobulins (pIg) across the mucosal epithelium. We report here that the human pIgR (hpIgR) can bind to a major pneumococcal adhesin, CbpA. Expression of hpIgR in human nasopharyngeal cells and MDCK cells greatly enhanced pneumococcal adherence and invasion. The hpIgR-mediated bacterial adherence and invasion were abolished by either insertional knockout of cbpA or antibodies against either hpIgR or CbpA. In contrast, rabbit pIgR (rpIgR) did not bind to CbpA and its expression in MDCK cells did not enhance pneumococcal adherence and invasion. These results suggest that pneumococci are a novel example of a pathogen co-opting the pIg transcytosis machinery to promote translocation across a mucosal barrier.
聚合免疫球蛋白受体(pIgR)通过将聚合免疫球蛋白(pIg)转运穿过黏膜上皮,在针对微生物感染的黏膜免疫中发挥关键作用。我们在此报告,人pIgR(hpIgR)可与主要的肺炎球菌黏附素CbpA结合。hpIgR在人鼻咽细胞和MDCK细胞中的表达极大地增强了肺炎球菌的黏附和侵袭。通过cbpA的插入敲除或针对hpIgR或CbpA的抗体,可消除hpIgR介导的细菌黏附和侵袭。相比之下,兔pIgR(rpIgR)不与CbpA结合,其在MDCK细胞中的表达也未增强肺炎球菌的黏附和侵袭。这些结果表明,肺炎球菌是病原体利用pIg转胞吞机制促进跨黏膜屏障转运的一个新例子。