IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia

被引:994
作者
Aujla, Shean J. [1 ]
Chan, Yvonne R. [2 ]
Zheng, Mingquan [1 ]
Fei, Mingjian [1 ]
Askew, David J. [3 ,4 ]
Pociask, Derek A. [1 ]
Reinhart, Todd A. [5 ]
McAllister, Florencia [1 ]
Edeal, Jennifer [1 ]
Gaus, Kristi [5 ]
Husain, Shahid [6 ]
Kreindler, James L. [1 ]
Dubin, Patricia J. [1 ]
Pilewski, Joseph M. [2 ]
Myerburg, Mike M. [2 ]
Mason, Carol A. [7 ]
Iwakura, Yoichiro [8 ]
Kolls, Jay K. [1 ]
机构
[1] Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA
[2] Univ Pittsburgh, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA 15213 USA
[3] Univ Pittsburgh, Med Ctr, Newborn Med Program, Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA
[4] Magee Womens Res Inst, Pittsburgh, PA 15213 USA
[5] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Infect Dis & Microbiol, Pittsburgh, PA 15261 USA
[6] Univ Pittsburgh, Med Ctr, Div Infect Dis, Transplant Infect Dis Unit, Pittsburgh, PA 15213 USA
[7] Louisiana Hlth Sci Ctr, Div Pulm & Crit Care Med, New Orleans, LA 70112 USA
[8] Univ Tokyo, Ctr Med Expt, Inst Med Sci, Minato Ku, Tokyo 1088639, Japan
关键词
D O I
10.1038/nm1710
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
Emerging evidence supports the concept that T helper type 17 (T(H)17) cells, in addition to mediating autoimmunity, have key roles in mucosal immunity against extracellular pathogens. Interleukin-22 (IL-22) and IL-17A are both effector cytokines produced by the T(H)17 lineage, and both were crucial for maintaining local control of the Gram-negative pulmonary pathogen, Klebsiella pneumoniae. Although both cytokines regulated CXC chemokines and granulocyte colony-stimulating factor production in the lung, only IL-22 increased lung epithelial cell proliferation and increased transepithelial resistance to injury. These data support the concept that the T(H)17 cell lineage and its effector molecules have evolved to effect host defense against extracellular pathogens at mucosal sites.
引用
收藏
页码:275 / 281
页数:7
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