PT  - JOURNAL ARTICLE
AU  - Gaëlle Rémy
AU  - Teddy Grandjean
AU  - Gwenola Kervoaze
AU  - Muriel Pichavant
AU  - Mathias Chamaillard
AU  - Philippe Gosset
TI  - Implication of interleukin-10 in the development of COPD induced by cigarette smoke exposure in mice
DP  - 2013 Sep 01
TA  - European Respiratory Journal
PG  - P614
VI  - 42
IP  - Suppl 57
4099  - http://erj.ersjournals.com/content/42/Suppl_57/P614.short
4100  - http://erj.ersjournals.com/content/42/Suppl_57/P614.full
SO  - Eur Respir J2013 Sep 01; 42
AB  - Background: Regulatory cytokines, such as interleukin-10 (IL-10), is essential to limit inflammation through the control of pro-inflammatory cytokines and the adaptative immunity. Chronic Obstructive Pulmonary Disease (COPD) is characterized by chronic inflammation of the airways leading to emphysema. In this disorder, it was shown that some COPD patients present a polymorphism of the Il10 – gene. This is associated with an altered secretion of IL-10 and correlated with a decline of lung function.Objectives: Our aim was to define the role of the IL-10 during the development of COPD, based on a mouse model of chronic exposure to cigarette smoke (CS).Methods: Balb/c wild type or IL-10-/- mice were daily exposed to CS. After 4 to 8 weeks of CS exposure, lung function was evaluated. Inflammation, cell recruitment, cytokine secretion and gene expression were analysed.Results: In WT mice, CS exposure induced lung inflammation, lung function changes and triggered the production of pulmonary IL-10. IL-10-deficient mice exposed to CS showed a higher recruitment of neutrophils and NKT cells, and a more altered decline in lung function compared to WT mice and to air-exposed IL-10-/- mice. Interestingly, pulmonary inflammation and lung function alteration appeared earlier in IL-10-/- mice. This was associated in the lungs with an increased production of IL-17 and MMP12, a metalloprotease known to be involved in pulmonary emphysema in COPD.Conclusion: These results suggest a protective role for IL-10 in COPD due to CS exposure. The cell sources of IL-10 and the mechanisms by which it controls the disease, remain to be determined.