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

Shean J. Aujla; Yvonne R. Chan; Mingquan Zheng; Mingjian Fei; David J. Askew; Derek A. Pociask; Todd A. Reinhart; Florencia McAllister; Jennifer Edeal; Kristi Gaus; Shahid Husain; James L. Kreindler; Patricia J. Dubin; Joseph M. Pilewski; Mike M. Myerburg; Carol A. Mason; Yoichiro Iwakura; Jay K. Kolls

doi:10.1038/nm1710

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

Shean J. Aujla, Yvonne R. Chan, Mingquan Zheng, Mingjian Fei, David J. Askew, Derek A. Pociask, Todd A. Reinhart, Florencia McAllister, Jennifer Edeal, Kristi Gaus, Shahid Husain, James L. Kreindler, Patricia J. Dubin, Joseph M. Pilewski, Mike M. Myerburg, Carol A. Mason, Yoichiro Iwakura, Jay K. Kolls

Research output: Contribution to journal › Article › peer-review

976 Scopus citations

Abstract

Emerging evidence supports the concept that T helper type 17 (T _H17) 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_H17 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_H17 cell lineage and its effector molecules have evolved to effect host defense against extracellular pathogens at mucosal sites.

Original language	English (US)
Pages (from-to)	275-281
Number of pages	7
Journal	Nature medicine
Volume	14
Issue number	3
DOIs	https://doi.org/10.1038/nm1710
State	Published - Mar 2008
Externally published	Yes

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

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Aujla, S. J., Chan, Y. R., Zheng, M., Fei, M., Askew, D. J., Pociask, D. A., Reinhart, T. A., McAllister, F., Edeal, J., Gaus, K., Husain, S., Kreindler, J. L., Dubin, P. J., Pilewski, J. M., Myerburg, M. M., Mason, C. A., Iwakura, Y., & Kolls, J. K. (2008). IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia. Nature medicine, 14(3), 275-281. https://doi.org/10.1038/nm1710

Aujla, SJ, Chan, YR, Zheng, M, Fei, M, Askew, DJ, Pociask, DA, Reinhart, TA, McAllister, F, Edeal, J, Gaus, K, Husain, S, Kreindler, JL, Dubin, PJ, Pilewski, JM, Myerburg, MM, Mason, CA, Iwakura, Y & Kolls, JK 2008, 'IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia', Nature medicine, vol. 14, no. 3, pp. 275-281. https://doi.org/10.1038/nm1710

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title = "IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia",

abstract = "Emerging evidence supports the concept that T helper type 17 (T H17) 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 TH17 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 TH17 cell lineage and its effector molecules have evolved to effect host defense against extracellular pathogens at mucosal sites.",

author = "Aujla, {Shean J.} and Chan, {Yvonne R.} and Mingquan Zheng and Mingjian Fei and Askew, {David J.} and Pociask, {Derek A.} and Reinhart, {Todd A.} and Florencia McAllister and Jennifer Edeal and Kristi Gaus and Shahid Husain and Kreindler, {James L.} and Dubin, {Patricia J.} and Pilewski, {Joseph M.} and Myerburg, {Mike M.} and Mason, {Carol A.} and Yoichiro Iwakura and Kolls, {Jay K.}",

note = "Funding Information: The authors would like to acknowledge support from the following Public Health Service grants: 5R01HL079142 (J.K.K.), P50HL084932, and P30DK072506 (J.K.K. and J.M.P.). We would like to thank Y. Iwakura (Center for Experimental Medicine, The Institute of Medical Science, The University of Tokyo) for the Il17a−/− mice, and T. Mak (University Health Network, Toronto) for the Lcn2−/− mice.",

year = "2008",

month = mar,

doi = "10.1038/nm1710",

language = "English (US)",

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pages = "275--281",

journal = "Nature medicine",

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AU - Aujla, Shean J.

AU - Chan, Yvonne R.

AU - Zheng, Mingquan

AU - Fei, Mingjian

AU - Askew, David J.

AU - Pociask, Derek A.

AU - Reinhart, Todd A.

AU - McAllister, Florencia

AU - Edeal, Jennifer

AU - Gaus, Kristi

AU - Husain, Shahid

AU - Kreindler, James L.

AU - Dubin, Patricia J.

AU - Pilewski, Joseph M.

AU - Myerburg, Mike M.

AU - Mason, Carol A.

AU - Iwakura, Yoichiro

AU - Kolls, Jay K.

N1 - Funding Information: The authors would like to acknowledge support from the following Public Health Service grants: 5R01HL079142 (J.K.K.), P50HL084932, and P30DK072506 (J.K.K. and J.M.P.). We would like to thank Y. Iwakura (Center for Experimental Medicine, The Institute of Medical Science, The University of Tokyo) for the Il17a−/− mice, and T. Mak (University Health Network, Toronto) for the Lcn2−/− mice.

PY - 2008/3

Y1 - 2008/3

N2 - Emerging evidence supports the concept that T helper type 17 (T H17) 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 TH17 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 TH17 cell lineage and its effector molecules have evolved to effect host defense against extracellular pathogens at mucosal sites.

AB - Emerging evidence supports the concept that T helper type 17 (T H17) 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 TH17 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 TH17 cell lineage and its effector molecules have evolved to effect host defense against extracellular pathogens at mucosal sites.

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

Abstract

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