Journal
EUROPEAN RESPIRATORY JOURNAL
Volume 33, Issue 2, Pages 375-381Publisher
EUROPEAN RESPIRATORY SOC JOURNALS LTD
DOI: 10.1183/09031936.00103408
Keywords
Airway infection; airway inflammation; animal; chemokines; cytokines
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The cholinergic nervous system can inhibit the systemic inflammation accompanying sepsis by virtue of a specific action of acetylcholine on alpha 7 cholinergic receptors. The current authors sought to determine the effect of nicotine, an alpha 7 cholinergic receptor agonist, on the host response to pneumonia caused by Streptococcus pneumoniae. Mice were intranasally infected with S. pneumoniae and treated with nicotine or saline intraperitoneally using a treatment schedule shown to improve host defence against abdominal sepsis. Nicotine treatment was associated with a transiently enhanced growth of S. pneumoniae, as indicated by higher bacterial loads in both lungs and blood at 24 h after infection. At 48 h after infection, bacterial burdens had increased in both treatment groups and differences were no longer present. Remarkably, mice treated with nicotine showed enhanced lung inflammation at 24 h after infection. Moreover, both lung and plasma concentrations of the pro-inflammatory cytokines tumour necrosis factor-alpha and interferon-gamma were higher in nicotine-treated animals at this time-point. Additional studies examining the effect of nicotine on the immediate (4-h) inflammatory response to S. pneumoniae did not reveal an anti-inflammatory effect of nicotine either. The present data suggest that nicotine transiently impairs host defence in pneumococcal pneumonia.
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