{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lee JJ"],"funding":["NCRR NIH HHS","NIEHS NIH HHS","NHLBI NIH HHS","NIAMS NIH HHS"],"pagination":["477-87"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4464693"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["135(2)"],"pubmed_abstract":["<h4>Background</h4>Contact toxicant reactions are accompanied by localized skin inflammation and concomitant increases in site-specific itch responses. The role(s) of eosinophils in these reactions is poorly understood. However, previous studies have suggested that localized eosinophil-nerve interactions at sites of inflammation significantly alter tissue innervation.<h4>Objective</h4>To define a potential mechanistic link between eosinophils and neurosensory responses in the skin leading to itching.<h4>Methods</h4>BALB/cJ mice were exposed to different contact toxicants, identifying trimellitic anhydride (TMA) for further study on the basis of inducing a robust eosinophilia accompanied by degranulation. Subsequent studies using TMA were performed with wild type versus eosinophil-deficient PHIL mice, assessing edematous responses and remodeling events such as sensory nerve innervation of the skin and induced pathophysiological responses (ie, itching).<h4>Results</h4>Exposure to TMA, but not dinitrofluorobenzene, resulted in a robust eosinophil skin infiltrate accompanied by significant levels of degranulation. Follow-up studies using TMA with wild type versus eosinophil-deficient PHIL mice showed that the induced edematous responses and histopathology were, in part, causatively linked with the presence of eosinophils. Significantly, these data also demonstrated that eosinophil-mediated events correlated with a significant increase in substance P content of the cutaneous nerves and an accompanying increase in itching, both of which were abolished in the absence of eosinophils.<h4>Conclusions</h4>Eosinophil-mediated events following TMA contact toxicant reactions increase skin sensory nerve substance P and, in turn, increase itching responses. Thus, eosinophil-nerve interactions provide a potential mechanistic link between eosinophil-mediated events and neurosensory responses following exposure to some contact toxicants."],"journal":["The Journal of allergy and clinical immunology"],"pubmed_title":["Eosinophil-dependent skin innervation and itching following contact toxicant exposure in mice."],"pmcid":["PMC4464693"],"funding_grant_id":["R01 AR061567","R01 ES017592","RR0109709","HL065228","ES017592","K26 RR019709","R01 ES014601","R56 HL058723","HL058723","[HL113023","R01 HL113023","R01 HL058723","R01 HL065228","AR061567","ES014601","F30 HL106930"],"pubmed_authors":["Protheroe CA","Kloeber JA","Jacoby NW","Raish RJ","Maizer P","Lee NA","Luo H","Jacoby DB","Dahl MV","Mazzolini A","Scott GD","Ochkur SI","Conley O","Neely JL","Lee JJ","Condjella RM","Zellner KR","Patel YS","Vega ML","Fryer AD"],"additional_accession":[]},"is_claimable":false,"name":"Eosinophil-dependent skin innervation and itching following contact toxicant exposure in mice.","description":"<h4>Background</h4>Contact toxicant reactions are accompanied by localized skin inflammation and concomitant increases in site-specific itch responses. The role(s) of eosinophils in these reactions is poorly understood. However, previous studies have suggested that localized eosinophil-nerve interactions at sites of inflammation significantly alter tissue innervation.<h4>Objective</h4>To define a potential mechanistic link between eosinophils and neurosensory responses in the skin leading to itching.<h4>Methods</h4>BALB/cJ mice were exposed to different contact toxicants, identifying trimellitic anhydride (TMA) for further study on the basis of inducing a robust eosinophilia accompanied by degranulation. Subsequent studies using TMA were performed with wild type versus eosinophil-deficient PHIL mice, assessing edematous responses and remodeling events such as sensory nerve innervation of the skin and induced pathophysiological responses (ie, itching).<h4>Results</h4>Exposure to TMA, but not dinitrofluorobenzene, resulted in a robust eosinophil skin infiltrate accompanied by significant levels of degranulation. Follow-up studies using TMA with wild type versus eosinophil-deficient PHIL mice showed that the induced edematous responses and histopathology were, in part, causatively linked with the presence of eosinophils. Significantly, these data also demonstrated that eosinophil-mediated events correlated with a significant increase in substance P content of the cutaneous nerves and an accompanying increase in itching, both of which were abolished in the absence of eosinophils.<h4>Conclusions</h4>Eosinophil-mediated events following TMA contact toxicant reactions increase skin sensory nerve substance P and, in turn, increase itching responses. Thus, eosinophil-nerve interactions provide a potential mechanistic link between eosinophil-mediated events and neurosensory responses following exposure to some contact toxicants.","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Feb","modification":"2026-05-02T05:15:18.153Z","creation":"2019-03-27T01:53:20Z"},"accession":"S-EPMC4464693","cross_references":{"pubmed":["25129680"],"doi":["10.1016/j.jaci.2014.07.003"]}}