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Cigarette smoke silences innate lymphoid cell function and facilitates an exacerbated type I interleukin-33-dependent response to infection.

Kearley, Jennifer ; Silver, Jonathan S ; Sandén, Caroline LU ; Liu, Zheng ; Berlin, Aaron A ; White, Natalie ; Mori, Michiko LU ; Pham, Tuyet-Hang ; Ward, Christine K and Criner, Gerard J , et al. (2015) In Immunity 42(3). p.566-579
Abstract
Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease and is presumed to be central to the altered responsiveness to recurrent infection in these patients. We examined the effects of smoke priming underlying the exacerbated response to viral infection in mice. Lack of interleukin-33 (IL-33) signaling conferred complete protection during exacerbation and prevented enhanced inflammation and exaggerated weight loss. Mechanistically, smoke was required to upregulate epithelial-derived IL-33 and simultaneously alter the distribution of the IL-33 receptor ST2. Specifically, smoke decreased ST2 expression on group 2 innate lymphoid cells (ILC2s) while elevating ST2 expression on macrophages and natural killer (NK)... (More)
Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease and is presumed to be central to the altered responsiveness to recurrent infection in these patients. We examined the effects of smoke priming underlying the exacerbated response to viral infection in mice. Lack of interleukin-33 (IL-33) signaling conferred complete protection during exacerbation and prevented enhanced inflammation and exaggerated weight loss. Mechanistically, smoke was required to upregulate epithelial-derived IL-33 and simultaneously alter the distribution of the IL-33 receptor ST2. Specifically, smoke decreased ST2 expression on group 2 innate lymphoid cells (ILC2s) while elevating ST2 expression on macrophages and natural killer (NK) cells, thus altering IL-33 responsiveness within the lung. Consequently, upon infection and release, increased local IL-33 significantly amplified type I proinflammatory responses via synergistic modulation of macrophage and NK cell function. Therefore, in COPD, smoke alters the lung microenvironment to facilitate an alternative IL-33-dependent exaggerated proinflammatory response to infection, exacerbating disease. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Immunity
volume
42
issue
3
pages
566 - 579
publisher
Cell Press
external identifiers
  • pmid:25786179
  • wos:000351301900019
  • scopus:84924981783
  • pmid:25786179
ISSN
1074-7613
DOI
10.1016/j.immuni.2015.02.011
language
English
LU publication?
yes
id
a0bf8e4a-4cb4-463b-a813-188a04518109 (old id 5258202)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25786179?dopt=Abstract
date added to LUP
2016-04-01 11:05:46
date last changed
2025-04-04 14:17:32
@article{a0bf8e4a-4cb4-463b-a813-188a04518109,
  abstract     = {{Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease and is presumed to be central to the altered responsiveness to recurrent infection in these patients. We examined the effects of smoke priming underlying the exacerbated response to viral infection in mice. Lack of interleukin-33 (IL-33) signaling conferred complete protection during exacerbation and prevented enhanced inflammation and exaggerated weight loss. Mechanistically, smoke was required to upregulate epithelial-derived IL-33 and simultaneously alter the distribution of the IL-33 receptor ST2. Specifically, smoke decreased ST2 expression on group 2 innate lymphoid cells (ILC2s) while elevating ST2 expression on macrophages and natural killer (NK) cells, thus altering IL-33 responsiveness within the lung. Consequently, upon infection and release, increased local IL-33 significantly amplified type I proinflammatory responses via synergistic modulation of macrophage and NK cell function. Therefore, in COPD, smoke alters the lung microenvironment to facilitate an alternative IL-33-dependent exaggerated proinflammatory response to infection, exacerbating disease.}},
  author       = {{Kearley, Jennifer and Silver, Jonathan S and Sandén, Caroline and Liu, Zheng and Berlin, Aaron A and White, Natalie and Mori, Michiko and Pham, Tuyet-Hang and Ward, Christine K and Criner, Gerard J and Marchetti, Nathaniel and Mustelin, Tomas and Erjefält, Jonas and Kolbeck, Roland and Humbles, Alison A}},
  issn         = {{1074-7613}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{566--579}},
  publisher    = {{Cell Press}},
  series       = {{Immunity}},
  title        = {{Cigarette smoke silences innate lymphoid cell function and facilitates an exacerbated type I interleukin-33-dependent response to infection.}},
  url          = {{http://dx.doi.org/10.1016/j.immuni.2015.02.011}},
  doi          = {{10.1016/j.immuni.2015.02.011}},
  volume       = {{42}},
  year         = {{2015}},
}