{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T22:11:23Z","timestamp":1790806283273,"version":"4.1.0"},"reference-count":35,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2024,7,2]],"date-time":"2024-07-02T00:00:00Z","timestamp":1719878400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["European Journal of Pain"],"published-print":{"date-parts":[[2024,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Visceral hypersensitivity is considered the core pathophysiological mechanism that causes abdominal pain in patients with irritable bowel syndrome (IBS). Fungal dysbiosis has been proved to contribute to visceral hypersensitivity in IBS patients. However, the underlying mechanisms for Dectin\u20101, a major fungal recognition receptor, in visceral hypersensitivity are poorly understood. This study aimed to explore the role of Dectin\u20101 in visceral hypersensitivity and elucidate the impact of Dectin\u20101 activity on the function of transient receptor potential vanilloid type 1 (TRPV1).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Visceral hypersensitivity model was established by the intracolonic administration of 0.1\u2009mL TNBS (130\u2009\u03bcg\/mL in 30% ethanol) in the male mice. Fluconazole and nystatin were used as fungicides. Laminarin, a Dectin\u20101 antagonist and gene knockout (\n                      <jats:italic>Clec7a<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>\u2212\/\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      ) mice were used to interrupt the function of Dectin\u20101. Colorectal distension\u2010electromyogram recording was performed to assess visceral sensitivity. Immunostaining experiment was performed to determine the localization of Dectin\u20101 in dorsal root ganglion (DRG) neurons. Calcium imaging study was performed to assay TRPV1\u2010mediated calcium influx in acutely dissociated DRG neurons.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Pretreatment with fungicides, administration of laminarin or genetic deletion of\n                      <jats:italic>Clec7a<\/jats:italic>\n                      alleviated TNBS\u2010induced visceral hypersensitivity in male mice. The expression of Dectin\u20101 was upregulated in the DRG and colon of TNBS\u2010treated mice. Colocalization of Dectin\u20101 and TRPV1 was observed in DRG neurons. Importantly, pretreatment with curdlan, a Dectin\u20101 agonist, increased TRPV1\u2010mediated calcium influx.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Dectin\u20101 contributes to visceral hypersensitivity in IBS or in inflammatory bowel disease in remission and activation of Dectin\u20101 induces TRPV1 sensitization.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance Statement<\/jats:title>\n                    <jats:p>This work provides direct evidence for the functional regulation of TRPV1 channel by Dectin\u20101 activity, proposing a new mechanism underlying TRPV1 sensitization. Control of intestinal fungi might be beneficial for the treatment of refractory abdominal pain in patients with IBS or IBD in remission.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ejp.2311","type":"journal-article","created":{"date-parts":[[2024,7,2]],"date-time":"2024-07-02T08:25:34Z","timestamp":1719908734000},"page":"1811-1826","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Dectin\u20101 induces\n                    <scp>TRPV1<\/scp>\n                    sensitization and contributes to visceral hypersensitivity of irritable bowel syndrome in male mice"],"prefix":"10.1002","volume":"28","author":[{"given":"Hao\u2010Nan","family":"Zheng","sequence":"first","affiliation":[{"name":"Department of Gastroenterology Peking University First Hospital  Beijing China"},{"name":"Department of Gastroenterology Peking University Third Hospital  Beijing 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Health Commission of China Peking University  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hao\u2010Zhou","family":"Zhang","sequence":"additional","affiliation":[{"name":"Neuroscience Research Institute, Department of Neurobiology, School of Basic Medical Sciences Peking University  Beijing China"},{"name":"Key Laboratory for Neuroscience, Ministry of Education\/National Health Commission of China Peking University  Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Feng","family":"Cao","sequence":"additional","affiliation":[{"name":"Neuroscience Research Institute, Department of Neurobiology, School of Basic Medical Sciences Peking University  Beijing China"},{"name":"Key Laboratory for Neuroscience, Ministry of Education\/National Health Commission of China Peking University  Beijing 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