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Marc Hershenson

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Primary Appointment: Pediatrics-Pulmonary Medicine
Primary PIBS Dept.: Molecular and Integrative Physiology
PubMed Name: Hershenson MB
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  My laboratory studies cellular and molecular mechanisms underlying chronic airways diseases such as asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis and bronchopulmonary dysplasia. At this time, we are focusing on two main projects.

First, we are studying the mechanisms by which rhinovirus (RV), a common cold virus, induces exacerbations of asthma and COPD. We recently found that Toll-like receptor (TLR)-2 is required for early inflammatory responses induced by rhinovirus, and that TLR2-positive macrophages are sufficient to confer airway inflammation to TLR2 knockout mice, with the pattern of inflammation depending on the macrophage activation state (Han et al. Journal of Allergy and Clinical Immunology 2016). This is surprising because TLR2 is a receptor for bacterial lipopeptides. We are now testing the novel hypothesis that insertion of RV myristoylated viral polypeptide (VP)-4 into the macrophage plasma membrane triggers cytokine production by interacting with a TLR2 signaling complex.

Second, we are studying the potential role of early-life viral infection in the initial development of asthma. We have found that rhinovirus (RV) infection of immature (6 day-old) but not mature mice increases lung IL-25 expression and expansion of IL-13-producing type 2 innate lymphoid cells (ILC2s), leading to an asthma-like phenotype including mucous hypersecretion and airways responsiveness (Hong et al. Journal of Allergy and Clinical Immunology 2014). We are now conducting further studies to understand the developmental regulation of viral-induced airway responses. Specifically, we are examining the roles of IL-25, IL-33 and TSLP in the development of the asthma phenotype, assessing the effects of RV in ILC2-deficient retinoic acid receptor-alpha knockout mice, and determining the effects of early-life RV infection on the response to secondary viral infection in later life.