Toggle Main Menu Toggle Search

Open Access padlockePrints

TNF-alpha in the regulation of MUC5AC secretion: Some aspects of cytokine-induced mucin hypersecretion on the in vitro model

Lookup NU author(s): Marina Smirnova, Professor Jeffrey Pearson

Downloads

Full text for this publication is not currently held within this repository. Alternative links are provided below where available.


Abstract

Tnf-α has been implicated in the aetiology of otitis media with effusion (OME), where goblet cells proliferate in a modified respiratory epithelium, leading to the accumulation of a mucin-rich effusion in the middle-ear cleft. The MUC5AC mucin gene product has been identified as a component of these effusions. Here we have used the HT29-MTX goblet cell line, which secretes MUC5AC mucin, as a model to study the effect of TNF-α on goblet cells. MUC5AC mucin was identified and quantitated with a monoclonal antibody NCL-HGM-45M1. TNF-α stimulates MUC5AC mucin secretion in a dose-dependent manner, with 20 ng/ml producing maximal stimulation. Both pre-confluent and confluent cells showed peak stimulation after 7 h, however the pre-confluent cells showed twice the level of mucin hypersecretion. These results suggest that TNF-α stimulation of mucin secretion could play an important role in the early acute phase of the development of OME. This hypersecretion of mucin could then lead to the failure of the mucociliary clearance system, resulting in the accumulation of a mucin-rich effusion in the middle ear and the movement to a more chronic phase of the disease. (C) 2000 Academic Press.


Publication metadata

Author(s): Smirnova MG; Pearson JP; Birchall JP

Publication type: Article

Publication status: Published

Journal: Cytokine

Year: 2000

Volume: 12

Issue: 11

Pages: 1732-1736

Print publication date: 01/01/2000

ISSN (print): 1043-4666

ISSN (electronic): 1096-0023

Publisher: Academic Press

URL: http://dx.doi.org/10.1006/cyto.2000.0763

DOI: 10.1006/cyto.2000.0763

PubMed id: 11052828


Altmetrics

Altmetrics provided by Altmetric


Share