@article {Ciprandi:March 1998:0954-7894:293,
	author = "Ciprandi,",
	author = "Ricca,",
	author = "Passalacqua,",
	author = "Fasolo,",
	author = "Canonica,",
	title = "Intranasal fluticasone propionate reduces ICAM-1 on nasal epithelial cells both during early and late phase after allergen challenge",
	journal = "Clinical & Experimental Allergy",
	volume = "28",
	year = "March 1998",
	abstract = "Background <P></P>Allergen specific nasal challenge (ASNC) is an optimal method to study the pathophysiological mechanisms sustaining the allergic inflammation and in particular the adhesion molecule system, which is involved in cellular infiltration of nasal mucosa. Topical steroids have been accepted as a highly effective anti-inflammatory therapy for allergic rhinitis. Objective <P></P>The aim of this double-blind placebo- controlled study was the evaluation of clinical and cytological parameters, including ICAM-1 expression on nasal epithelial cells, after a 4&#8201;week treatment with nasal fluticasone propionate (200 &#956;g/daily) or placebo, using the model of ASNC. Methods <P></P>Twenty allergic rhinitics underwent nasal challenge before and after treatment. The following parameters were evaluated: (i) nasal symptoms (rhinorrhoea, itching, sneezing, obstruction), (ii) inflammatory cells (eosinophils and neutrophils), (iii) ICAM-1 expression on nasal epihelial cells at baseline, 30&#8201;min (early phase) and 6&#8201;h (late phase) after ASNC. Results <P></P>Fluticasone propionate was capable of reducing: (i) clinical symptoms during both early (<I>P&#8201;</I>&#60;&#8201;0.001) and late phase (<I>P&#8201;</I>&#60;&#8201;0.04), (ii) eosinophil (<I>P&#8201;</I>&#60;&#8201;0.002) and neutrophil (<I>P&#8201;</I>&#60;&#8201;0.001) infiltrate during late phase, and (iii) ICAM-1 expression on nasal epithelial cells during both early (<I>P&#8201;</I>&#60;&#8201;0.01) and late phase (<I>P&#8201;</I>&#60;&#8201;0.03). Conclusions <P></P>The present results demonstrate that fluticasone propionate exerts a significant action on early and late phase clinical events following specific nasal challenge, reducing also the cellular influx during the late phase. This event is likely due to the modulation of ICAM-1 expression on epithelial cells.",
	pages = "293-299(7)",
	url = "http://www.ingentaconnect.com/content/bsc/cea/1998/00000028/00000003/art00007"
	doi = "doi:10.1046/j.1365-2222.1998.00239.x"
}