{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T23:12:31Z","timestamp":1777417951586,"version":"3.51.4"},"reference-count":47,"publisher":"European Respiratory Society (ERS)","issue":"4","content-domain":{"domain":["publications.ersnet.org"],"crossmark-restriction":true},"short-container-title":["Eur Respir J"],"accepted":{"date-parts":[[2014,8,26]]},"published-print":{"date-parts":[[2015,4]]},"abstract":"<jats:p>Prostaglandin D<jats:sub>2<\/jats:sub>(PGD<jats:sub>2<\/jats:sub>) causes cough and levels are increased in asthma suggesting that it may contribute to symptoms. Although the prostaglandin D<jats:sub>2<\/jats:sub>receptor 2 (DP<jats:sub>2<\/jats:sub>) is a target for numerous drug discovery programmes little is known about the actions of PGD<jats:sub>2<\/jats:sub>on sensory nerves and cough.<\/jats:p><jats:p>We used human and guinea pig bioassays,<jats:italic>in vivo<\/jats:italic>electrophysiology and a guinea pig conscious cough model to assess the effect of prostaglandin D<jats:sub>2<\/jats:sub>receptor (DP<jats:sub>1<\/jats:sub>), DP<jats:sub>2<\/jats:sub>and thromboxane receptor antagonism on PGD<jats:sub>2<\/jats:sub>responses.<\/jats:p><jats:p>PGD<jats:sub>2<\/jats:sub>caused cough in a conscious guinea pig model and an increase in calcium in airway jugular ganglia. Using pharmacology and receptor-deficient mice we showed that the DP<jats:sub>1<\/jats:sub>receptor mediates sensory nerve activation in mouse, guinea pig and human vagal afferents.<jats:italic>In vivo<\/jats:italic>, PGD<jats:sub>2<\/jats:sub>and a DP<jats:sub>1<\/jats:sub>receptor agonist, but not a DP<jats:sub>2<\/jats:sub>receptor agonist, activated single airway C-fibres. Interestingly, activation of DP<jats:sub>2<\/jats:sub>inhibited sensory nerve firing to capsaicin<jats:italic>in vitro<\/jats:italic>and<jats:italic>in vivo<\/jats:italic>.<\/jats:p><jats:p>The DP<jats:sub>1<\/jats:sub>receptor could be a therapeutic target for symptoms associated with asthma. Where endogenous PGD<jats:sub>2<\/jats:sub>levels are elevated, loss of DP<jats:sub>2<\/jats:sub>receptor-mediated inhibition of sensory nerves may lead to an increase in vagally associated symptoms and the potential for such adverse effects should be investigated in clinical studies with DP<jats:sub>2<\/jats:sub>antagonists.<\/jats:p>","DOI":"10.1183\/09031936.00061614","type":"journal-article","created":{"date-parts":[[2014,10,17]],"date-time":"2014-10-17T10:08:52Z","timestamp":1413540532000},"page":"1108-1118","update-policy":"https:\/\/doi.org\/10.1183\/ers-crossmark-policy","source":"Crossref","is-referenced-by-count":49,"title":["Prostaglandin D<sub>2<\/sub>and the role of the DP<sub>1<\/sub>, DP<sub>2<\/sub>and TP receptors in the control of airway reflex events"],"prefix":"10.1183","volume":"45","author":[{"given":"Sarah A.","family":"Maher","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mark 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