This Article Full Text Full Text (PDF) All Versions of this Article: 2006-0404OCv1 37/5/606    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hauber, H.-P. Articles by Zabel, P. Search for Related Content PubMed PubMed Citation Articles by Hauber, H.-P. Articles by Zabel, P.

Effect of Dexamethasone and ACC on Bacteria-Induced Mucin Expression in Human Airway Mucosa

¹ Medical Clinic, and ² Department of Pathology, Research Center Borstel, Borstel, Germany; and ³ ENT Department, University Hospital Schleswig Holstein Campus Lübeck, Lübeck, Germany

Correspondence and requests for reprints should be addressed to Hans-Peter Hauber, M.D., Medical Clinic, Research Center Borstel, Parkallee 35, 23845 Borstel, Germany. E-mail: hphauber{at}web.de

Gram-negative bacteria can stimulate mucin production, but excessive mucus supports bacterial infection and consequently leads to airway obstruction. Therefore, the effect of dexamethasone (DEX) and the antioxidant acetyl-cysteine (ACC) on bacteria-induced mucus expression was investigated. Explanted human airway mucosa and mucoepidermoid cells (Calu-3) were stimulated with lipopolysaccharide (LPS) or PAM3 (a synthetic lipoprotein). DEX or ACC were added to either LPS- or PAM3-stimulated airway mucosa or Calu-3 cells. Mucin mRNA expression (MUC5AC) and total mucus glycoconjugates (mucin protein) were quantified using real-time PCR and periodic acid Schiff staining. LPS and PAM3 significantly increased mucin expression in airway mucosa and Calu-3 cells (P < 0.05). DEX alone had no significant effect on mucin expression in airway mucosa or Calu-3 cells (P > 0.05). In contrast, DEX significantly reduced LPS- and PAM3-induced mucin expression in explanted mucosal tissue and mucin expression in Calu-3 cells (P < 0.05). In explanted human airway mucosa ACC alone significantly increased mucin expression (P < 0.05). In contrast, ACC significantly decreased LPS- and PAM3-induced mucin expression (P < 0.05). In Calu-3 cells ACC alone had no significant effect on mucin expression (P > 0.05). ACC decreased LPS- and PAM3-induced mucin expression, but this effect was not significant (P > 0.05). These data suggest that DEX can effectively reduce bacteria-induced mucin expression in the airways. ACC alone may increase mucin expression in noninfected mucosa, but it decreased bacteria-induced mucin expression. Further studies are warranted to evaluate whether the effect of DEX or ACC is clinically relevant.

Key Words: acetyl-cysteine • dexamethasone • lipoprotein • lipopolysaccharide • mucin