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Cigarette Smoke Alters Lungs’ Inflammatory Response

Last Updated: April 13, 2009.

Exposure to cigarette smoke exacerbates and skews the respiratory system's inflammatory response to bacteria in mice, which may shed light on smoking's role in the development of inflammation in chronic obstructive pulmonary disease in humans, researchers report in the April 15 issue of the American Journal of Respiratory and Critical Care Medicine.

MONDAY, April 13 (HealthDay News) -- Exposure to cigarette smoke exacerbates and skews the respiratory system's inflammatory response to bacteria in mice, which may shed light on smoking's role in the development of inflammation in chronic obstructive pulmonary disease (COPD) in humans, researchers report in the April 15 issue of the American Journal of Respiratory and Critical Care Medicine.

Gordon J. Gaschler, of McMaster University in Hamilton, Ontario, Canada, and colleagues exposed mice to cigarette smoke twice daily, five days per week for eight weeks. The mice were then exposed to non-typeable Haemophilus influenzae bacteria, a pathogen implicated in COPD exacerbations. A control group of smoke-free mice was also exposed to the bacteria. The mice were harvested and lung tissue and bronchoalveolar lavage fluid were examined.

Pulmonary inflammation and lung damage were greater in the smoke-exposed mice compared with the smoke-free control mice, the investigators found. The smoke-exposed mice exhibited a worsened histological appearance, increased hydroxyproline, and a skewed inflammatory mediator response marked by up-regulation of a different subset of inflammatory mediators than the control mice, in particular MCP-1, -3, and -5, IP-10, and MIP-1γ. The researchers also found that corticosteroids attenuated inflammation in both groups, although this appeared to increase bacterial burden.

"Altogether, this study highlights that inflammatory pathways may be altered during COPD, which should be taken into consideration for the design of therapeutic interventions for COPD and COPD exacerbation," the authors write.

Two of the study authors report they are employed by AstraZeneca, and one author received a grant from AstraZeneca that funded the study in part.

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