A mechanism of antigen-induced mucus production in nasal epithelium of sensitized rats - A comparison with lipopolysaccharide-induced mucus production

We produced ovalbumin (OVA)-sensitized rats as an animal model of nasal all ergy. Intranasal instillation of OVA induced hypertrophic and metaplastic c hanges of goblet cells in nasal epithelium of OVA- sensitized rats. Intraep ithelial mucosubstance in nasal mucosa increased significantly at 24 h afte r 3 or 7 d of OVA instillation, accompanied by mucosal infiltration of eosi nophils, The effects of H1-antagonist (d-chlorpheniramine malate), H2-antag onist (cimetidine), dexamethasone, indomethacin, cysteinyl leukotrienes (cy s-LTs)-antagonist (ONO1078), and antirat neutrophil antiserum on OVA-induce d changes were examined. Mucus production was significantly inhibited by de xamethasone, and ONO1078, whereas eosinophil infiltration was significantly inhibited by H1-antagonist, dexamethasone, and anti-rat neutrophil antiser um. These results indicate that cysLTs (LTs C4, D4, and E4) may play an imp ortant role in antigen-induced mucus production, and that eosinophil infilt ration does not relate to mucus production. Intranasal instillation of lipo polysaccharide (LPS) also induced intraepithelial mucus production, and it was significantly inhibited by dexamethasone, indomethacin, and antirat neu trophil antiserum; however, cysLTs antagonist had no effect on LPS-induced change. These results indicate that neutrophil and cyclooxygenase products are important in LPS-induced mucus production, and there are different mech anisms of mucus production between allergic inflammation and LPS stimulatio n.