Middle ear mucosa is a modified respiratory epithelium and five genes for secreted mucins (MUCs 2, 3, 4, 5AC, 5B and 8) are expressed in the airways. In this study we have compared the composition predicted by the gene sequences of these mucins with that of mucins isolated from middle ear effusions. Three groups of mucins, (1) thick and (2) thin from anatomically normal children and (3) effusions from children with a cleft palate were studied. Amino acid analysis was performed on glycopeptide fragments corresponding to the characteristic tandem repeat domains of cloned mucin genes. There were marked differences both between the three mucin pools and from the tandem repeat sequences of the five cloned genes expressed in the airways. Serine, threonine and proline contributed 44%, 29% and 36% from groups (1) (2) and (3)respectively, in the ratios (2.4 : 2.9 : 1) (5 : 1 : 1) and (3.5 : 1 : 1.5).The serine to threonine ratio in thick effusions is similar to that found in MUC 4; however, the high proportion of serine in mucin from groups (2) and (3) is novel. Therefore, more than one mucin gene product is secreted by the human middle ear mucosa and further mucin genes expressed by the middle ear are yet to be cloned.
A function of nasal turbinates is the removal of particles bythe action of the cilia moving a mucous blanket. The rheologicalproperties of the mucous secretion are critical to this functionand dependent on several factors, in particular the integrity and type of mucin present. Recent work has shown that MUC5AC is a major secreted mucin in the respiratory tract and MUC2 is expressed at a much lower level.1,2 Alteration in the levels of expression of mucin genes could potentially alter the transport and lubricating properties of mucous. mRNA was isolated from inferior nasal turbinates and electrophoresis showed a polydisperse mRNA population. Northern blots were probed with 48bp digoxigenin labelled antisense oligonucleotides to the tandem repeat sequences of MUC2 and MUC5AC. The MUC2 probe gave an intense signal with the positive control (human ileum), in contrast the negative control (rat kidney) showed no binding. Turbinate mRNA also gave a strong signal although not as intense as ileum. The MUC5AC probe bound to turbinate mRNA and ileum although to a lesser extent than MUC2. The results show that both MUC2 and MUC5AC are expressed in human nasal turbinates and interestingly the level ofMUC2 was higher than that of MUC5AC (using these probes). This reversal in mucin secretory pattern, presumablya function of hyperplasia could lead to altered mucous properties. This tissue may provide a good model to study diseases in tissues of the same embryological origin and similar histology where cell proliferative changes occur, i.e. diseases of middle ear mucosa. We thank the Hearing Research Trust for their support.
Mucins are responsible for the high viscosity of middle ear effusions preventing clearance from the middle ear. Nine mucin genes (MUC genes) have been identified. We have shown at least two biochemically distinct mucins are present in OME and ELISA studies showed no reactivity with MUC1 or MUC2, suggesting low levels of MUC5AC and higher levels of MUC5B. Here we have investigated further immuno histochemically to determine the cellular localization of these gene products. Rabbit polyclonal antisera (TEPA2) were raised to highly purified mucin from thick effusions. The monoclonal antibody NCL‐HGM‐45M1 was used to probe for MUC5AC. Surgical tissue specimens were fixed in 10% formal saline overnight, wax embedded and sectioned (5 μm). Microwave retrieval was followed with primary antibody then by biotinylated secondary antibody followed by AB complexing and haematoxylin counterstaining (see Table 1). There was no staining of non‐mucus secreting cells in test or control tissues. The pattern of staining with TEPA2 in salivary glands, trachea, stomach, and ileum matched that previously reported for MUC5B.1 MUC5AC (NCL‐HGM‐45M1) was not present in middle ear mucosa but was present in goblet cells of nasal turbinates and probably reflects a low expression of MUC5AC as seen from low levels present in the effusion (5–15% by weight of mucin). TEPA2 stained the mucous glands of middle ear mucosa but not the goblet cells. Based on TEPA2 staining MUC5B is therefore a strong candidate for the mucin produced by middle ear mucosal glands, studies continue to confirm this and to determine the gene product of the goblet cells.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.