Host resistance to lung infection mediated by major vault protein in epithelial cells

被引：107

作者：

Kowalski, Michael P.

Dubouix-Bourandy, Anne

Bajmoczi, Milan

Golan, David E.

Zaidi, Tanweer

Coutinho-Sledge, Yamara S.

Gygi, Melanie P.

Gygi, Steven P.

Wiemer, Erik A. C.

Pier, Gerald B. ^{[1
]}

机构：

[1] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Channing Lab, Boston, MA 02115 USA

[2] Novartis Inst Biomed Res, Cambridge, MA 02139 USA

[3] Inst Federatif Biol Purpan, Lab Bacteriol Hyg, Toulouse, France

[4] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA

[5] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA

[6] Brigham & Womens Hosp, Dept Med, Div Hematol, Boston, MA 02115 USA

[7] Erasmus MC, Josephine Nefkens Inst, Dept Med Oncol, NL-3015 GE Rotterdam, Netherlands

来源：

SCIENCE | 2007年 / 317卷 / 5834期

关键词：

D O I：

10.1126/science.1142311

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

The airway epithelium plays an essential role in innate immunity to lung pathogens. Ribonucleoprotein particles primarily composed of major vault protein (MVP) are highly expressed in cells that encounter xenobiotics. However, a clear biologic function for MVP is not established. We report here that MVP is rapidly recruited to lipid rafts when human lung epithelial cells are infected with Pseudomonas aeruginosa, and maximal recruitment is dependent on bacterial binding to the cystic fibrosis transmembrane conductance regulator. MVP was also essential for optimal epithelial cell internalization and clearance of P. aeruginosa. These results suggest that MVP makes a substantial contribution to epithelial cell-mediated resistance to infection.

引用

页码：130 / 132

页数：3

共 30 条

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