Rationale The rise in asthma has been attributed to a number of risk factors including poor eating habits such as high sugar intake, especially in children. Interactions between molecular and cellular components of the pulmonary innate immune system such as the carbohydrate recognition molecule surfactant protein-D (SP-D) and dendritic cells may regulate susceptibility to airway inflammatory diseases. We hypothesize that a high sucrose diet impairs the immunoprotective action of SP-D and increases susceptibility to airway inflammation. Methods C57BL/6 and SP-D deficient mice were studied. A short-term (overnight) high sugar consumption-induced murine model of intermittent hyperglycemia was combined with a well-established model of allergic sensitization and challenge using Aspergillus fumigatus (Af) extract. Cellular inflammation, lung function, cytokine and SP-D levels in the airways of mice on sugar diet were compared to animals receiving normal diet during allergic sensitization and challenge. Results Compared with wild-type mice, SP-D deficient animals displayed increased baseline glucose levels and developed elevated serum IgE in response to sensitization with Af. In Af-sensiticed wild type mice, high sucrose diet induced intermittent spikes of hyperglycaemia, significantly enhanced levels of TNFa, increased number of dendritic cells and eosinophilic inflammation 36 hours after Af challenge. Further, sensitized mice on sucrose developed a significant eosinophilia and elevated lung resistance even without allergen challenge. Unlike mice on normal diet, sucrose-fed mice did not up-regulate SP-D protein in the BAL 36 hrs after allergen challenge. Conclusion A sugar rich diet may prime the innate immune system of the airways to allergic inflammation.
Full conference title:
2008 American Academy of Allergy, Asthma, and Immunology Annual Meeting
- AAAAI 2008 (64th)