SEP 09, 2020 10:00 AM PDT

Immunoprotective vs. immunopathogenic responses during fungal-associated allergic airway inflammation

Sponsored by: LUMINEX
C.E. Credits: P.A.C.E. CE Florida CE
Speaker
  • Professor and Chair, Department of Microbiology and Immunology Tulane University
    Biography

      The current goals of my research are to better understand lung immune responses during acute vs. chronic exposure to the opportunistic fungal pathogen Aspergillus fumigatus. During acute exposure, which is an infection model mimicking invasive pulmonary aspergillosis, our major focus is on the cytokine IL-22. Specifically, we investigate pathways that positively and negatively regulate IL-22 production as well as the antifungal immune pathways induced by IL-22. Themes in this area of investigation include common γ-chain cytokines, innate lymphocytes and eicosanoid biology. An important shift in my laboratory over the last several years has been focused on the identification of inflammatory biomarkers, immune cells and pathways in human lung diseases that correlate with functional decline, and bringing these observations back to experimental animal models to provide mechanistic insight (i.e. bedside-to-bench). To this end, during chronic exposure, which is a model of severe asthma with fungal sensitization as well as chronic fungal exposure during diseases such as cystic fibrosis, our major focus is on various inflammatory mediators we have identified in human subjects. Themes in this area of investigation include various IL-1 family members, unique chemokines and chitinases/chitinase-like proteins.


    Abstract

    Asthma is an increasing health concern affecting more than 25 million individuals in the United States and more than 300 million individuals worldwide. In some cases, sensitization or exposure to specific microbes can exacerbate asthma. In 2006, a new asthma phenotype termed “severe asthma with fungal sensitization” (SAFS) was described for individuals whose asthma was poorly-controlled and who were sensitized to fungi. We have previously reported that asthmatics sensitized to fungi demonstrate worse lung function, higher serum IgE, blood eosinophil and exhaled nitric oxide levels. A growing area of interest is the identification of factors that contribute to immunopathogenesis in allergic asthma, including those sensitized to fungi, and determining whether these could be viable therapeutic targets. Indeed, biologics targeting the type 2 cytokines IL-4, IL-5 and IL-13 have been successful in treating individuals with severe asthma. To this end, we have reported that human asthmatics sensitized to fungi have increased levels of multiple cytokines, chemokines and growth factors in bronchoalveolar lavage fluid and sputum, some of which correlate with lung function or atopic measurements. This presentation will provide an overview of these findings and how some of these mediators mechanistically contribute to disease severity using an experimental animal model of fungal-associated allergic airway inflammation.

    Learning Objectives:

    1. To understand the clinical significance of allergic asthma as it relates to fungal sensitization

    2. To understand experimental animal models as it relates to determining immunoprotective vs. immunopathogenic responses during fungal asthma


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