The role of Proton-sensing ovarian cancer G protein-coupled receptor 1 in a murine asthma model.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25860635
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Respiratory organ internal medicine
• Research Institution: Gunma University
• Principal Investigator: AOKI HARUKA 群馬大学, 生体調節研究所, 助教 (80447268)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 気管支喘息 / アレルギー

Outline of Final Research Achievements

OGR1 stimulation by extracellular protons causes the activation of G proteins and subsequent cellular functions. In the present study, we show that OGR1-deficient mice are resistant to the cardinal features of asthma, including airway eosinophilia, airway hyperresponsiveness, and goblet cell metaplasia, in association with a remarkable inhibition of Th2 cytokine and IgE productionl. Intratracheal transfer to wild-type mice of OVA-primed bone marrow-derived dendritic cells (DCs) from OGR1-deficient mice developed lower AHR and eosinophilia after OVA inhalation compared with the transfer of those from wild-type mice. Migration of OVA-pulsed DCs to peribronchial lymph nodes was also inhibited by OGR1 deficiency in the adoption experiments. OVA-induced expression of CCR7, a mature DC chemokine receptor, and migration response to CCR7 ligands in an in vitro Transwell assay were attenuated by OGR1 deficiency.

Free Research Field

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