{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T23:39:46Z","timestamp":1790033986028,"version":"4.0.1"},"reference-count":43,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2017,8,7]],"date-time":"2017-08-07T00:00:00Z","timestamp":1502064000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neurogastroenterology Motil"],"published-print":{"date-parts":[[2018,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>The role of immune activation in Functional Dyspepsia (<jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content>) patients without previous infection is unclear. We compare the gastric and circulating brain\u2010derived neurotropic factor (<jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content>), receptor potential vanilloid type (<jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>) families and various cytokines in <jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content> patients.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Consecutive adult <jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content> patients (Rome <jats:styled-content style=\"fixed-case\">III<\/jats:styled-content>) with no recent history of gastroenteritis and asymptomatic healthy controls were recruited for upper endoscopy. Subjects with <jats:styled-content style=\"fixed-case\">GERD<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">IBS<\/jats:styled-content> as predominant symptoms, diabetes mellitus, current or previous <jats:italic>Helicobacter pylori<\/jats:italic> infection, psychiatric illness and recent use of <jats:styled-content style=\"fixed-case\">NSAID<\/jats:styled-content> or <jats:styled-content style=\"fixed-case\">PPI<\/jats:styled-content> were excluded. Corpus biopsies and serum samples were collected.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>Forty three [M:F=8:35, mean age: 35.0 (9.3)] <jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content> patients were compared with 23 healthy controls [M:F=8:15, mean age: 36.6 (10.2)]. <jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content> patients had postprandial distress syndrome (<jats:styled-content style=\"fixed-case\">PDS<\/jats:styled-content>) as predominant sub\u2010type (<jats:styled-content style=\"fixed-case\">PDS<\/jats:styled-content>: 36, <jats:styled-content style=\"fixed-case\">EPS<\/jats:styled-content>: 2). There was no significant difference in the median inflammation score (<jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content>:0 (0\u20101) vs Control:0 (0\u20101), <jats:italic>P<\/jats:italic>=.79). However, <jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content> patients had significantly higher <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> expression of <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>1 (<jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content>:0.014\u00b10.007, Control:0.003\u00b10.001, 4.6 fold, <jats:italic>P<\/jats:italic>=.02) and <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>2 (<jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content>:0.012\u00b10.006, Control:0.003\u00b10.001, 4 fold, <jats:italic>P<\/jats:italic>=.02) compared to controls. The serum (<jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content>:258.0\u00b112.3\u00a0ng\u00a0ml<jats:sup>\u22121<\/jats:sup>, Control:319.7\u00b118.1\u00a0ng\u00a0ml<jats:sup>\u22121<\/jats:sup>, <jats:italic>P<\/jats:italic>&lt;.01) and gastric <jats:styled-content style=\"fixed-case\">BDNF mRNA<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content>:0.06\u00b10.008, Control:0.092\u00b10.01, 0.65 fold, <jats:italic>P<\/jats:italic>=.02)levels significantly lower in <jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content> patients. Secretion of cytokines (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20104, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20105, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201010, G\u2010<jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> TGF<\/jats:styled-content>\u2010\u03b22, <jats:styled-content style=\"fixed-case\">MCP<\/jats:styled-content>\u20101)was also highly correlated with dyspeptic symptoms in patients with FD.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions &amp; Inferences<\/jats:title><jats:p>Despite lacking gastric mucosal inflammation, up\u2010regulation of <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>1 and <jats:styled-content style=\"fixed-case\">TRPV<\/jats:styled-content>2, down\u2010regulation of <jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content> were observed in <jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content> patients. These suggest that immune alteration may contribute to the pathogenesis of <jats:styled-content style=\"fixed-case\">FD<\/jats:styled-content> without any previous infection.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nmo.13176","type":"journal-article","created":{"date-parts":[[2017,8,7]],"date-time":"2017-08-07T06:46:36Z","timestamp":1502088396000},"source":"Crossref","is-referenced-by-count":27,"title":["Up\u2010regulation of transient receptor potential vanilloid (<scp>TRPV<\/scp>) and down\u2010regulation of brain\u2010derived neurotrophic factor (<scp>BDNF<\/scp>) expression in patients with functional dyspepsia (<scp>FD<\/scp>)"],"prefix":"10.1111","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2415-6600","authenticated-orcid":false,"given":"C. K. Y.","family":"Cheung","sequence":"first","affiliation":[{"name":"Institute of Digestive Disease The Chinese University of Hong Kong  Hong Kong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L. L.","family":"Lan","sequence":"additional","affiliation":[{"name":"Institute of Digestive Disease The Chinese University of Hong Kong  Hong Kong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Kyaw","sequence":"additional","affiliation":[{"name":"Institute of Digestive Disease The Chinese University of Hong Kong  Hong Kong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. D. P.","family":"Mak","sequence":"additional","affiliation":[{"name":"Department of Psychiatry The Chinese University of Hong Kong  Hong Kong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Chan","sequence":"additional","affiliation":[{"name":"Department of Anatomical Cellular and Pathology The Chinese University of Hong Kong  Hong Kong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y.","family":"Chan","sequence":"additional","affiliation":[{"name":"Institute of Digestive Disease The Chinese University of Hong Kong  Hong Kong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. C. 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