The kinin B1 receptor mediates alloknesis in a murine model of inflammation

•Non-noxious mechanical stimulus elicits itch in skin inflamed by complete Freund's adjuvant.•Subcutaneous naltrexone reduces alloknesis score.•Premedication with kinin B1 receptor antagonist reduces alloknesis score.•Premedication with kinin B2 receptor antagonist increases alloknesis score. Noxious stimuli and non-noxious mechanical stimuli elicit itch (alloknesis) instead of pain on skin lesions of patients with atopic dermatitis. We previously found that bradykinin evokes an itch-related scratching response through activation of kinin B1 receptor in skin inflamed using complete Freund's adjuvant. In this study we investigated whether alloknesis is evoked in CFA-inflamed skin and the involvement of kinin receptors. In our results, alloknesis was elicited four days after CFA-inflammation. Furthermore, pretreatment with a B1 receptor antagonist or μ-opioid receptor antagonist significantly reduced alloknesis. In contrast, treatment with a B2 receptor antagonist significantly increased alloknesis. These results suggest that the alloknesis response is mediated by the activation of kinin B1 receptor but antagonized by the B2 receptor in CFA-inflamed mice.