Observed in the presence of BK in primary dorsal root ganglia
Observed in the presence of BK in primary dorsal root ganglia (DRG) culture [8]. Whether BK participates in the chronic itch progress directly on the peripheral nerve endings or indirectly is not known. It is known, however, that B1R and BK?2015 Liu et al. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http:// EPZ004777 chemical information creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/ zero/1.0/) applies to the data made available in this article, unless otherwise stated.Liu et al. Mol Pain (2015) 11:Page 2 ofreceptor 2 (B2R) are G protein-coupled receptors that mediate kinin effects. In normal skin, B2R signaling predominates, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25609842 however, and cutaneous inflammation results in enhanced B1R responses. Our previous studies have shown that itching is induced by BK, and the activation of kinin B1 receptor mediates the alloknesis response in complete Freund’s adjuvant (CFA)-inflamed mice [9]. At the same time, in the epithelium of patients with asthma, B1R is up regulated and associated with airborne allergens that may play a role in the pathophysiology of atopic and allergic diseases [10]. Stadnicki has suggested that B1R mRNA and protein increase in specimens from inflammatory bowel disease (IBD) patients and the enhanced B1R expression is related to the pathology of IBD [11, 12]. Nevertheless, a litter study on the itching sensation reported high B1R expression, focused on chronic itching in AD. Whether the expression of B1R changes and whether B1R expression is related to the etiology and development of the itching sensation in a chronic inflammatory state remains unclear. A recent report has indicated that treatment with diphenylcyclopropenone (DCP) often results in contact dermatitis, as well as intense itching, in both humans and mice [13, 14]. If this is the case, DCP-treated mice can be considered as a chronic inflammatory in vitro model. We focus on B1R function on itching behaviors in DCPtreated mice. In the present study, we evaluated scratching behaviors in a PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27872238 mouse model of AD, especially focusing on (1) whether B1R affects itching behaviors and peripheral sensory neurons directly, and (2) its possible regulatory mechanism in up regulating B1R. For this purpose, we investigated the significance of B1R based on the behavior of the animal model and the skin tissuesdetected by immunohistochemistry. We then explored the possible regulatory activity of B1R by correlating B1R expression with keratinocytes dysfunction. We also tried to find out whether B1R is an independent factor in differentiating and proliferating in chronic inflammatory conditions.ResultsAntagonism of B1R significantly inhibited scratching in DCPtreated animals, while selective antagonist of B2R did notPruritus symptoms produced following repeated application of 1 DCP (Aldrich Chemical Co, Milwaukee, WI, USA) was characterized by a pronounced and long-lasting increase in spontaneous scratching behavior by the hind paw (Fig. 1a). This process was observed starting on day 3, reaching a maximum on day 10 after repeated application of 1 DCP on the seventh day (the results were not shown). Interestingly, preventive.
