Dexamethasone suppresses mucus production and MUC-2 and MUC-5AC gene expression by NCI-H292 cells

Kai, Hirofumi; Yoshitake, Kazuhisa; Hisatsune, Akinori; Kido, Teruhiko; Isohama, Yoichiro; Takahama, Kazuo; Miyata, Takeshi

doi:10.1152/ajplung.1996.271.3.l484

Cited by 67 publications

(65 citation statements)

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“…Pretreatment with 40 M of quercetin and 20 M of EGCG decreased mucin gene expression, and cell proliferation was not influenced at any of the concentrations. These results agree with the suppression of MUC2 and MUC5AC expression by dexamethasone in NCI-H292 cells 14 and that of IL-1␤-induced MUC2/5AC expression and mucin production by budesonide. 21,22 Our results also agree with other studies on the suppression of the mucin gene by [6]-gingerol and EGCG.…”

Section: Discussionsupporting

confidence: 90%

Dietary Polyphenols Affect Muc5Ac Expression and Ciliary Movement in Respiratory Cells and Nasal Mucosa

Chang

Song

Kim

et al. 2010

Am J Rhinol�Allergy

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Section: Discussionsupporting

confidence: 90%

Dietary Polyphenols Affect Muc5Ac Expression and Ciliary Movement in Respiratory Cells and Nasal Mucosa

Chang

Song

Kim

et al. 2010

Am J Rhinol�Allergy

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“…Since airway inflammation is key to the development of mucus hypersecretion [44], the inhibitory actions of budesonide may not be entirely unexpected. In addition, direct effects of glucocorticosteroids on mucin gene expression have been reported in vitro [45]. In combination with the results obtained using tiotropium bromide, these data indicate that glucocorticosteroids and anticholinergic drugs may both be effective in preventing remodelling of mucus-producing cells in allergic airways disease.…”

Section: Discussionmentioning

confidence: 52%

Inhibition of allergen-induced airway remodelling by tiotropium and budesonide: a comparison

Bos¹,

Gosens²,

Zuidhof³

et al. 2007

European Respiratory Journal

193

166

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Chronic inflammation in asthma and chronic obstructive pulmonary disease drives pathological structural remodelling of the airways. Using tiotropium bromide, acetylcholine was recently identified as playing a major regulatory role in airway smooth muscle remodelling in a guinea pig model of ongoing allergic asthma. The aim of the present study was to investigate other aspects of airway remodelling and to compare the effectiveness of tiotropium to the glucocorticosteroid budesonide.Ovalbumin-sensitised guinea pigs were challenged for 12 weeks with aerosolised ovalbumin. The ovalbumin induced airway smooth muscle thickening, hypercontractility of tracheal smooth muscle, increased pulmonary contractile protein (smooth-muscle myosin) abundance, mucous gland hypertrophy, an increase in mucin 5 subtypes A and C (MUC5AC)-positive goblet cell numbers and eosinophilia. It was reported previously that treatment with tiotropium inhibits airway smooth muscle thickening and contractile protein expression, and prevents tracheal hypercontractility. This study demonstrates that tiotropium also fully prevented allergen-induced mucous gland hypertrophy, and partially reduced the increase in MUC5AC-positive goblet cell numbers and eosinophil infiltration. Treatment with budesonide also prevented airway smooth muscle thickening, contractile protein expression, tracheal hypercontractility and mucous gland hypertrophy, and partially reduced MUC5AC-positive goblet cell numbers and eosinophilia.This study demonstrates that tiotropium and budesonide are similarly effective in inhibiting several aspects of airway remodelling, providing further evidence that the beneficial effects of tiotropium bromide might exceed those of bronchodilation.

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“…Kai et al (44) showed that dexamethasone suppressed mucin release directly from a lung carcinoma cell line, most likely as a result of inhibition of mucin synthesis. Kim et al showed that cationic peptides such as eosinophil major basic protein (45) and poly-L-lysine and poly-L-arginine (46) suppress mucin release from primary hamster TSE cells without cytotoxicity.…”

Section: Agents That Regulate Airway Goblet Cell Mucin Releasementioning

confidence: 99%

Pharmacology of Airway Goblet Cell Mucin Release

et al. 2003

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Abstract. Airway mucus hypersecretion is one of the major clinical manifestations of patients suffering from various pulmonary diseases. However, no drugs are yet available to control airway mucus hypersecretion. For the past 15 years, a plethora of information has amassed with regard to the pharmacology of airway goblet cell mucin secretion using various primary cell culture systems. The recent discovery of various MUC genes has also greatly stimulated research in this field. Nevertheless, the heterogeneity of the oligosaccharide structure of mucin molecules makes it extremely difficult to assess the significance of the information derived from the pharmacological studies. Therefore, it seems crucially important to understand the roles of individual mucins in conjunction with normal airway physiology and pathology, which should be the future research directions necessary for studying airway goblet cell mucin pharmacology.

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Dexamethasone suppresses mucus production and MUC-2 and MUC-5AC gene expression by NCI-H292 cells

Cited by 67 publications

References 0 publications

Dietary Polyphenols Affect Muc5Ac Expression and Ciliary Movement in Respiratory Cells and Nasal Mucosa

Dietary Polyphenols Affect Muc5Ac Expression and Ciliary Movement in Respiratory Cells and Nasal Mucosa

Inhibition of allergen-induced airway remodelling by tiotropium and budesonide: a comparison

Pharmacology of Airway Goblet Cell Mucin Release

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