{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T11:37:45Z","timestamp":1791286665452,"version":"4.1.0"},"reference-count":24,"publisher":"SAGE Publications","issue":"5","license":[{"start":{"date-parts":[[2006,9,1]],"date-time":"2006-09-01T00:00:00Z","timestamp":1157068800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Rhinology"],"published-print":{"date-parts":[[2006,9]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Histamine, a key chemical mediator in allergic reaction, exhibits an array of pro-inflammatory effects that include the activation of fibroblasts. The aim of this study was to evaluate whether histamine could stimulate nasal polyp-derived fibroblasts to express vascular cell adhesion molecule (VCAM)-1, a surface molecule involved in structural-inflammatory cell interaction and whether levocetirizine could inhibit this induction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Primary nasal polyp tissue-derived fibroblasts were stimulated with histamine (10\u20131000 \u03bcM) or interleukin (IL)-4 plus tumor necrosis factor (TNF)-\u03b1 (0.5\u20135 ng\/mL) and VCAM-1 expression was evaluated by flow cytometry analysis. The inhibitory effect of the selective H\n                      <jats:sub>1<\/jats:sub>\n                      -antagonist levocetirizine (0.01\u201310.0\u03bcM) on VCAM-1 expression was also tested.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Compared with unstimulated cultures, histamine or IL-4 + TNF-\u03b1, at the highest concentrations tested, significantly increase VCAM-1 expression (p &lt; 0.05). To evaluate the ability of levocetirizine to downregulate VCAM-1 expression, fibroblasts were stimulated with histamine (1000 \u03bcM) or IL-4 + TNF-\u03b1 (5 ng\/mL), in the presence of the drug (0.01\u201310.0 \u03bcM). The histamine-induced VCAM-1 expression was effectively inhibited by levocetirizine (0.1\u201310.0 \u03bcM) (p &lt; 0.05). No effect of the drug on IL-4 + TNF-\u03b1-induced VCAM-1 expression was observed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Histamine upregulates VCAM-1 expression on nasal polyp-derived fibroblasts and this phenomenon, relevant to allergic late-phase inflammation, is effectively inhibited by levocetirizine.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2500\/ajr.2006.20.0796","type":"journal-article","created":{"date-parts":[[2006,10,9]],"date-time":"2006-10-09T19:10:17Z","timestamp":1160421017000},"page":"445-449","source":"Crossref","is-referenced-by-count":16,"title":["The Histamine-Induced Enhanced Expression of Vascular Cell Adhesion Molecule-1 by Nasal Polyp-Derived Fibroblasts is Inhibited by Levocetirizine"],"prefix":"10.1177","volume":"20","author":[{"given":"Loredana","family":"Petecchia","sequence":"first","affiliation":[{"name":"Pulmonary Disease Unit, G. Gaslini Institute, Genoa, Italy"},{"name":"Immunohematology and Transfusion Medicine Service, G. Gaslini Institute, Genoa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura","family":"Serpero","sequence":"additional","affiliation":[{"name":"Pulmonary Disease Unit, G. Gaslini Institute, Genoa, Italy"},{"name":"Immunohematology and Transfusion Medicine Service, G. Gaslini Institute, Genoa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michela","family":"Silvestri","sequence":"additional","affiliation":[{"name":"Pulmonary Disease Unit, G. Gaslini Institute, Genoa, Italy"},{"name":"Immunohematology and Transfusion Medicine Service, G. Gaslini Institute, Genoa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Federica","family":"Sabatini","sequence":"additional","affiliation":[{"name":"Pulmonary Disease Unit, G. Gaslini Institute, Genoa, Italy"},{"name":"Immunohematology and Transfusion Medicine Service, G. Gaslini Institute, Genoa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucia","family":"Scarso","sequence":"additional","affiliation":[{"name":"Pulmonary Disease Unit, G. Gaslini Institute, Genoa, Italy"},{"name":"Immunohematology and Transfusion Medicine Service, G. Gaslini Institute, Genoa, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giovanni A.","family":"Rossi","sequence":"additional","affiliation":[{"name":"Pulmonary Disease Unit, G. Gaslini Institute, Genoa, Italy"},{"name":"Immunohematology and Transfusion Medicine Service, G. 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