Alveolar Macrophages Mediate Allergic Airway Inflammation In The Obese-asthma Models
Authors: J.Y. Kim, J.H. Sohn, J.H. Lee, C.S. Hong, J.W. Park
Journal: Journal of Allergy and Clinical Immunology (2011)

RATIONALE: Obesity associated with the pathogenesis of several inflammatory disorders is a known risk factor for allergic asthma. In the inflammatory reactions, macrophages are important for the phagocytosis, antigen presentation, and proinflammatory cytokines secretion. Alveolar macrophages encountered inhaled-allergens are vital to the development of allergic asthma and are central factors in the pathological interaction between obesity and asthma. In this study, we investigated whether alveolar macrophages and their TNF-α production could affect airway inflammation in the obese-asthma models.METHODS: We generated obese C57BL/6 mice by high-fat-feeding and then cockroach allergen-induced asthma models of the obese mice (obese-asthma model). These obese-asthma models treated with a Cl2MDP-containing liposome for alveolar macrophages deficient. The effects of alveolar macrophages deficient on the pathopysiological and immunological responses of the obese-asthma models were analyzed.RESULTS: The obese-asthma models increased the airway hyperresponsiveness (AHR) and the tumor necrosis factor (TNF)-α producing-cells population in the lung tissue compared to the lean-asthma models. Depression of the alveolar macrophages in the obese-asthma models had decreased the development of the AHR, the macrophages infiltration in the bronchoalveolar lavage fluid and the TNF-α producing-cells population in the lung tissue compared to the lean-asthma models.CONCLUSIONS: These results suggest that obesity partially enhances the cockroach-induced asthma, and the alveolar macrophages and their TNF-α production may affect the development of asthma. RATIONALE: Obesity associated with the pathogenesis of several inflammatory disorders is a known risk factor for allergic asthma. In the inflammatory reactions, macrophages are important for the phagocytosis, antigen presentation, and proinflammatory cytokines secretion. Alveolar macrophages encountered inhaled-allergens are vital to the development of allergic asthma and are central factors in the pathological interaction between obesity and asthma. In this study, we investigated whether alveolar macrophages and their TNF-α production could affect airway inflammation in the obese-asthma models. METHODS: We generated obese C57BL/6 mice by high-fat-feeding and then cockroach allergen-induced asthma models of the obese mice (obese-asthma model). These obese-asthma models treated with a Cl2MDP-containing liposome for alveolar macrophages deficient. The effects of alveolar macrophages deficient on the pathopysiological and immunological responses of the obese-asthma models were analyzed. RESULTS: The obese-asthma models increased the airway hyperresponsiveness (AHR) and the tumor necrosis factor (TNF)-α producing-cells population in the lung tissue compared to the lean-asthma models. Depression of the alveolar macrophages in the obese-asthma models had decreased the development of the AHR, the macrophages infiltration in the bronchoalveolar lavage fluid and the TNF-α producing-cells population in the lung tissue compared to the lean-asthma models. CONCLUSIONS: These results suggest that obesity partially enhances the cockroach-induced asthma, and the alveolar macrophages and their TNF-α production may affect the development of asthma.