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GPR91 deficiency exacerbates allergic contact dermatitis while reducing arthritic disease in mice
T Rubić-Schneider1,2, N Carballido-Perrig1,2, C Regairaz1
1Novartis Institutes for Biomedical Research (NIBR), Basel, Switzerland.
Allergy
|August 17, 2016
Summary
Mice lacking succinate sensing (Sucnr1) showed heightened allergic contact dermatitis and mast cell activation. However, this did not worsen asthma or arthritis, suggesting GPR91 antagonists could treat these diseases.
Area of Science:
- Immunology
- Metabolism
- Allergy & Inflammation
Background:
- Succinate acts as an alarmin, signaling tissue injury and inflammation.
- Its role in allergic and inflammatory responses is not fully understood.
Purpose of the Study:
- To investigate the role of succinate receptor 1 (SUCNR1/GPR91) in allergic contact dermatitis (ACD).
- To evaluate the impact of succinate sensing on mast cell development and inflammatory conditions like asthma and arthritis.
Main Methods:
- Compared ear thickness in wild-type and Sucnr1-deficient mice challenged with oxazolone for ACD.
- Assessed mast cell activation in vitro and in vivo.
- Utilized passive cutaneous anaphylaxis, ovalbumin-induced asthma, and arthritis models.
Main Results:
- Sucnr1-deficient mice exhibited augmented ACD reactions and increased mast cell activation.
- Exacerbated mast cell activation in deficient mice did not enhance asthma or arthritis.
- Hyperactive mast cell phenotype resulted from developmental alterations in the absence of succinate.
Conclusions:
- Succinate sensing deficiency during mast cell development leads to a hyperactive phenotype.
- This hyperactivity does not exacerbate mast cell-dependent asthma or arthritis.
- Sucnr1-deficient mice showed reduced arthritis, indicating GPR91 antagonists may treat allergic and autoimmune diseases.
