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ARS Home » Northeast Area » Beltsville, Maryland (BARC) » Beltsville Agricultural Research Center » Animal Parasitic Diseases Laboratory » Research » Publications at this Location » Publication #365565

Research Project: Immune, Molecular, and Ecological Approaches for Attenuating GI Nematode Infections of Ruminants

Location: Animal Parasitic Diseases Laboratory

Title: TRPV4 is dispensable for the development of airway allergic asthma

item PALANIYANDI, SENTHILKUMAR - University Of Maryland
item RAJENDRAKUMAR, ARUNRAJ - University Of Maryland
item PERIASAMY, SIVAKUMAR - Albany Medical College
item GOSWAMI, RISHOV - University Of Maryland
item Tuo, Wenbin
item ZHU, XIAOPING - University Of Maryland
item RAHAMAN, SHAIK - University Of Maryland

Submitted to: Laboratory Investigation
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/23/2019
Publication Date: 8/15/2019
Citation: Palaniyandi, S., Rajendrakumar, A.M., Periasamy, S., Goswami, R., Tuo, W., Zhu, X., Rahaman, S.O. 2019. TRPV4 is dispensable for the development of airway allergic asthma. Laboratory Investigation.

Interpretive Summary: Mucosal immune responses determine how infections in the gut and lung are resolved. To better understand and manage gastrointestinal parasites of livestock, USDA scientists partnered with University immunologists to explore the contribution of a particular protein to inflammation engendering allergic airway asthma. Such allergic asthma was demonstrated not to require transient receptor potential cation channel subfamily V member 4, a protein previously found to promote lung fibrosis in chronic asthma. These data shed light on the pathogenesis of an important lung disease, and may help explain the cascade of pathogenesis induced by gastrointestinal parasitic nematodes in cattle. These insights will be of interest to allergists, pathologists, physicians, molecular immunologists, parasitologists, and veterinarians.

Technical Abstract: Airway allergic asthma is one of the most common immune-mediated disorders affecting the lungs. Allergic asthma is characterized clinically by airway hyperresponsiveness, eosinophilia, enhanced IL4 and IL13, peribronchial inflammation with mononuclear cells, and goblet cell hyperplasia associated with increased mucus production. However, chronic asthma with repeated exposures to airway allergens can result in subepithelial pulmonary fibrosis. The transient receptor potential cation channel subfamily V member 4 (TRPV4) protein can promote the generation of myofibroblasts and pulmonary fibrosis. Here, we investigated the possibility that TPRV4 facilitates the development of airway allergic asthma and subsequent pulmonary fibrosis in the lung. To test this, wild-type (WT) and TPRV4 gene knockout (KO) mice were repeatedly sensitized with chicken ovalbumin (OVA) and repeatedly subjected to aerosol challenge with 1% OVA. We found that there were no significant differences in the development of airway allergic asthma between the WT and TPRV4 KO mice. Both groups of mice exhibited similar levels of airway hyperresponsiveness, and levels of IL13, IL5, OVA-specific IgE, eosinophilia, mucus-secreting goblet cell hyperplasia, and deposition of collagen fiber, a hallmark of the pulmonary fibrosis. Thus, these data suggest that TPRV4 protein is dispensable in development and pathogenesis of airway asthma and subsequent fibrosis.