Dr. Cory Hogaboam’s  major research interests encompass mechanisms that regulate immune and inflammatory events during allergy and asthma. We recently developed a chronic model of A. fumigatus-induced airway inflammation that exhibits the characteristic pulmonary phenotype of asthmatics, incorporating local and systemic allergic inflammation associated with a chronic pulmonary eosinophilia, elevated IgE levels, reversible airway obstruction, goblet cell hyperplasia and peribronchial fibrosis. Although some of these features are present in other murine models of allergic airway disease, the advantage of this fungal asthma model is its chronicity (i.e. responses lasting months rather than hours). In addition, given that live fungal conidia initiate the allergic disease, this model also lends itself to exploring the aspects of chemokine biology that are required for an efficient anti-fungal response while avoiding the devastating consequences of acquired allergic responsiveness. At present, we have examined the contribution of CC chemokine receptors-1 (CCR1), CCR2, CCR4, CCR5 and CCR8 in the development and maintenance of chronic fungal asthma. The individual contribution of each receptor has been explored in the context of genetically altered mice that lack the appropriate chemokine receptor due to homologous recombination or gene knockout. These studies have provided several unique findings including the startling revelation that, at least in vivo, chemokine receptors have defined, non-redundant roles in the innate, effector, and remodeling responses associated with allergic airway disease. Taken together, these studies have revealed the complex and specific roles of chemokines and chemokine receptors during fungal asthma, and should lead to the identification of anti-chemokine strategies that ameliorate all features of chronic fungal asthma without compromising the innate immune response against A. fumigatus conidia.

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