Eustachian tube gland tissue changes are related to bacterial species in acute otitis media

Abstract

Background and objective: Prior investigations have shown that the number of mucus producing goblet cells in the middle ear and Eustachian tube (ET) mucosa is highly increased during and up to at least six months after experimental acute otitis media (AOM) caused by Streptococcus pneumoniae (SP). Further, the volume of the mucus producing paratubal gland components is increased up to 3 months after the acute infection. These changes may in conjunction with a deteriorated ET function predispose a subsequent development of secretory otitis media. The present investigation compares changes in goblet cell density and gland structures of the ET during and after AOM caused by various bacteria typically encountered in this disease, with emphasis on potential differences due to bacterial species. Methods: Rat models of AOM caused by SP, non-typeable or type b Haemophilus influenzae (NTHI/HIB) or Moraxella catarrhalis (MC) were studied longitudinally up to 6 months after bacterial challenge. The ET was dissected and decalcified, paraffin embedded and serially sectioned, followed by PAS/alcian blue staining. The goblet cell density and the paratubal gland composition and volume were determined morphometrically in every 20th section, using a light microscope. Results: Regardless of bacterial species, the ET goblet cell density was increased from day 8 and peaked day 16, followed by some degree of normalisation, although not reaching normal numbers within the 6 month period, except for MC. The highest increase was seen in AOM caused by the non-typeable Haemophilus strain, followed by HIB, SP and MC. Except with MC, pathological intra-epithelial glands formed and goblet cells were found in mucosal areas normally devoid of these. In all species but MC, the volume of the paratubal glands progressed to peak 16 days post-inoculation, followed by a gradual normalisation. The volume was still increased 3 months after the acute infection, but completely normalised after 6 months. The increase was primarily due to hypertrophy of the mucous gland components and highest in AOM caused by the Haemophilus species, followed by SP. Conclusion: The Eustachian tube goblet cell density is increased during and up to at least six months after AOM regardless of bacterial species, except when employing MC, by which the density was increased for a few weeks only. Except in AOM caused by MC, the volume of the ET glands increases during and up to at least 3 months after infection, primarily due to hypertrophy of the mucous gland components. The non-typeable Haemophilus strain induced the highest increase of both goblet cell density and mucous gland volume. The increased secretory capacity of the ET following AOM may by excessive mucus secretion contribute to the deteriorated ET function found after AOM and thus predispose, sustain or aggravate middle ear disease.