Contribution of the Th-17 pathway in lung inflammation response in F508del-CFTR mice
(2012) 26th annual North American Cystic Fibrosis Conference — Location: Orlando, FL (11.October.2012)
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- Abstract
- Objectives: The exuberant lung inflammatory response in CF has long been recognized as a neutrophil-dominated process. More recently, attention has been drawn to the contribution of other immune cell populations into the progressive lung tissue damage in CF e.g. macrophages. However, little is known about the role played by lymphocytes. The recent observation of increased levels of the proinflammatory IL-17, secreted by T helper 17 (Th17) cells, in the bronchoalveolar lavage (BAL) of CF patients undergoing pulmonary exacerbation, raised the assumption that Th17 pathway may play a central role in CF lung disease. This work aimed at investigating the contribution of Th-17 in lung inflammatory responses in the CF mouse model. Methods: We characterized, by qRT-PCR and ELISA, the in-vivo molecular inflammatory environment in lungs of normal and homozygous F508del-CFTR mice in basal conditions and after endotracheal instillation of lipopolysaccharide from Pseudomonas aeruginosa (LPS). We showed here that basal mRNA expression levels of IL-17A, IL-17F and IL-22 were barely detected in lungs from CF and non-CF mice, with, as expected, no detectable levels of the corresponding interleukins in BAL. Interestingly, IL-17A, IL-17F and IL-22 mRNA after LPS instillation were found to be higher in the CF group than in the normal group. These data were in agreement with those monitored at the protein level, as IL-17A and IL-22 responses were detected in BAL from CF but barely from normal. Th- 17-related cytokines (IL-1β, IL-6, IL-23, GM-CSF) were similarly induced by LPS in both genotypes. Conclusion: Our results showed that responses to LPS of Th-17-related factors are exaggerated in CF mice.
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Noël, S., Dhooghe, B., Huaux, F., Lebecque, P., Wallemacq, P., & Leal, T. (2012). Contribution of the Th-17 pathway in lung inflammation response in F508del-CFTR mice. Pediatric Pulmonology, 47(S35), 272. https://hdl.handle.net/2078.5/205955 (Original work published 2012)