Labeling of the glucocorticoid receptor and Na,K-ATPase in a rat otitis media model

Citation
M. Hultcrantz et al., Labeling of the glucocorticoid receptor and Na,K-ATPase in a rat otitis media model, AM J OTOL, 21(1), 2000, pp. 36-41
Citations number
20
Categorie Soggetti
Otolaryngology
Journal title
AMERICAN JOURNAL OF OTOLOGY
ISSN journal
01929763 → ACNP
Volume
21
Issue
1
Year of publication
2000
Pages
36 - 41
Database
ISI
SICI code
0192-9763(200001)21:1<36:LOTGRA>2.0.ZU;2-R
Abstract
Hypothesis: Glucocorticoid hormones exert an influence on the inflammatory response of the middle ear during acute otitis media. Rats with experimenta lly induced purulent otitis media were given either glucocorticoid hormones in excess or a glucocorticoid hormone blocker that deprived the animals of the hormone. Background: Acute otitis media is a common inflammatory disease among child ren. Streptococcus pneumoniae is the most usual causative agent. The standa rd treatment today is phenoxymethylpenicillin. The role of glucocorticoid h ormones in inflammatory reactions in the middle ear has been widely debated . Methods: In an otitis media model, a suspension of pneumococci was inoculat ed into the bulla of the rat, after the animals were pretreated with either a dose of corticosteroid hormones or the glucocorticoid receptor blocking agent RU 486. Rats with induction of otitis media only, but no pretreatment , were used as control subjects, as were the left control-operated ears of all rats. The inflammatory response in the inner ear and in the middle ear was evaluated. The presence of glucocorticoid receptors and the enzyme Na,K -ATPase was investigated with immunohistochemistry. Results: The inflammatory response in the animals with untreated otitis med ia and in the group with otitis media in rats pretreated with the receptor blocker was much more extensive than in the group of animals pretreated wit h corticosteroids. In the corticosteroid-treated group, the tympanic membra ne and the mucous membrane of the middle ear were less edematous, but the m iddle ear cavity contained more pus. Only a few lymphocytes were found in t he inner ears of these rats. When the inner ear was labeled with antibodies against glucocorticoid receptors, there seemed to be no difference between the labeling patterns in the three groups. This was also the case for anti body labeling against Na,K-ATPase. Conclusion: The present results indicate that the reaction in the middle ea r mucous membrane is more pronounced in rats that had been pretreated with the hormone receptor blocking drug. An increase of corticosteroid hormone l evels during the inflammatory process seem to diminish the reaction in the tympanic membrane and the middle ear mucosa. Neither the hormone receptor b locking drug nor the steroid hormones change the content of glucorticoid re ceptors and Na,K-ATPase in the inner ear in the otitis media rat model.