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Cigarette smoke attenuates the nasal host response to Streptococcus pneumoniae and predisposes to invasive pneumococcal disease in mice.

Shen, Pamela; Morissette, Mathieu C; Vanderstocken, Gilles; Gao, Yang; Hassan, Muhammad; Roos, Abraham LU ; Thayaparan, Danya; Merlano, Maria; Dorrington, Michael G and Nikota, Jake K, et al. (2016) In Infection and Immunity 84(5). p.1536-1547
Abstract
Streptococcus pneumoniae is a leading cause of invasive bacterial infections, with nasal colonization an important first step for disease. While cigarette smoking is a strong risk factor for invasive pneumococcal disease, underlying mechanisms remain unknown. This is partly due to a lack of clinically relevant animal models investigating nasal pneumococcal colonization in the context of cigarette smoke exposure. We present a model of nasal pneumococcal colonization in cigarette smoke-exposed mice and document, for the first time, that cigarette smoke predisposes to invasive pneumococcal infection and mortality in an animal model. Cigarette smoke increased the risk of bacteraemia and meningitis without prior lung infection. Mechanistically,... (More)
Streptococcus pneumoniae is a leading cause of invasive bacterial infections, with nasal colonization an important first step for disease. While cigarette smoking is a strong risk factor for invasive pneumococcal disease, underlying mechanisms remain unknown. This is partly due to a lack of clinically relevant animal models investigating nasal pneumococcal colonization in the context of cigarette smoke exposure. We present a model of nasal pneumococcal colonization in cigarette smoke-exposed mice and document, for the first time, that cigarette smoke predisposes to invasive pneumococcal infection and mortality in an animal model. Cigarette smoke increased the risk of bacteraemia and meningitis without prior lung infection. Mechanistically, deficiency in IL-1α or PAFR, an important host receptor thought to bind and facilitate pneumococcal invasiveness, did not rescue cigarette smoke-exposed mice from invasive pneumococcal disease. Importantly, we observed cigarette smoke to attenuate nasal inflammatory mediator expression, particularly that of neutrophil recruiting chemokines, normally elicited by pneumococcal colonization. Smoking cessation during nasal pneumococcal colonization rescued nasal neutrophil recruitment and prevented invasive disease in mice. We propose that cigarette smoke predisposes to invasive pneumococcal disease by suppressing inflammatory processes of the upper respiratory tract. Given that smoking prevalence remain high worldwide, these findings are relevant to the continued efforts to reduce invasive pneumococcal disease burden. (Less)
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publication status
published
subject
in
Infection and Immunity
volume
84
issue
5
pages
1536 - 1547
publisher
American Society for Microbiology
external identifiers
  • pmid:26930709
  • scopus:84965115594
  • wos:000377106600027
ISSN
1098-5522
DOI
10.1128/IAI.01504-15
language
English
LU publication?
yes
id
d72a35e2-8c70-4327-9462-591dc8ccb96d (old id 8856678)
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http://www.ncbi.nlm.nih.gov/pubmed/26930709?dopt=Abstract
date added to LUP
2016-03-15 10:28:58
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2017-10-01 03:13:50
@article{d72a35e2-8c70-4327-9462-591dc8ccb96d,
  abstract     = {Streptococcus pneumoniae is a leading cause of invasive bacterial infections, with nasal colonization an important first step for disease. While cigarette smoking is a strong risk factor for invasive pneumococcal disease, underlying mechanisms remain unknown. This is partly due to a lack of clinically relevant animal models investigating nasal pneumococcal colonization in the context of cigarette smoke exposure. We present a model of nasal pneumococcal colonization in cigarette smoke-exposed mice and document, for the first time, that cigarette smoke predisposes to invasive pneumococcal infection and mortality in an animal model. Cigarette smoke increased the risk of bacteraemia and meningitis without prior lung infection. Mechanistically, deficiency in IL-1α or PAFR, an important host receptor thought to bind and facilitate pneumococcal invasiveness, did not rescue cigarette smoke-exposed mice from invasive pneumococcal disease. Importantly, we observed cigarette smoke to attenuate nasal inflammatory mediator expression, particularly that of neutrophil recruiting chemokines, normally elicited by pneumococcal colonization. Smoking cessation during nasal pneumococcal colonization rescued nasal neutrophil recruitment and prevented invasive disease in mice. We propose that cigarette smoke predisposes to invasive pneumococcal disease by suppressing inflammatory processes of the upper respiratory tract. Given that smoking prevalence remain high worldwide, these findings are relevant to the continued efforts to reduce invasive pneumococcal disease burden.},
  author       = {Shen, Pamela and Morissette, Mathieu C and Vanderstocken, Gilles and Gao, Yang and Hassan, Muhammad and Roos, Abraham and Thayaparan, Danya and Merlano, Maria and Dorrington, Michael G and Nikota, Jake K and Bauer, Carla Mt and Kwiecien, Jacek M and Labiris, Renee and Bowdish, Dawn Me and Stevenson, Christopher S and Stämpfli, Martin R},
  issn         = {1098-5522},
  language     = {eng},
  month        = {02},
  number       = {5},
  pages        = {1536--1547},
  publisher    = {American Society for Microbiology},
  series       = {Infection and Immunity},
  title        = {Cigarette smoke attenuates the nasal host response to Streptococcus pneumoniae and predisposes to invasive pneumococcal disease in mice.},
  url          = {http://dx.doi.org/10.1128/IAI.01504-15},
  volume       = {84},
  year         = {2016},
}