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

Eustachian tube gland tissue changes are related to bacterial species in acute otitis media
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DOI:
10.1016/j.ijporl.2003.09.010
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发表时间:
2004-01-01
影响因子:
1.5
通讯作者:
Tos, M
Tos, M
中科院分区:
医学4区
文献类型:
--
作者:
Cayé-Thomasen, P;Tos, M

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背景与目的:以往的研究表明,肺炎链球菌(SP)所致的实验性急性中耳炎(AOM)后中耳和咽鼓管黏膜中产生粘液的杯状细胞数量显著增加,至少6个月以上。此外,在急性感染后3个月,产生输卵管旁腺体成分的粘液的体积增加。这些变化可能与ET功能恶化一起导致分泌性中耳炎的后续发展。本研究比较了由本病常见的各种细菌引起的AOM过程中和AOM后ET的杯状细胞密度和腺体结构的变化,重点是由于细菌种类的潜在差异。方法:对SP、非分型或b型流感嗜血杆菌(NTHI/HIB)或卡他莫拉菌(MC)所致大鼠急性呼吸窘迫综合征(AOM)模型进行纵向研究,直至细菌攻击后6个月。解剖脱钙,石蜡包埋,连续切片,PAS/爱先蓝染色。在光镜下对每20个切片的杯状细胞密度、输卵管旁腺的组成和体积进行了形态计量学测定。结果:无论细菌种类如何,ET杯状细胞密度从第8天开始增加,第16天达到高峰,随后有一定程度的正常化,但在6个月内仍未达到正常数量,MC除外。非分型嗜血杆菌引起的AOM增加最多,其次是HIB、SP和MC。除MC外,病理性上皮内腺形成,在通常缺乏这些腺体的粘膜区域可见杯状细胞。在除MC外的所有物种中,输卵管旁腺体的体积在接种后16天达到峰值,随后逐渐正常化。急性感染后3个月血容量仍增加,6个月后完全恢复正常。增加的原因主要是由于粘液腺成分的肥大,其中以嗜血杆菌引起的AOM增加最多,其次是SIR。结论:在AOM后至少6个月,咽鼓管杯状细胞密度增加,除了使用MC时,密度只增加了几周。除MC引起的AOM外,ET腺体体积在感染后至少3个月内增大,主要是由于粘液腺成分肥大。非分型嗜血杆菌诱导的杯状细胞密度和粘液腺体积增加幅度最大。AOM后ET分泌能力的增加可能是由于粘液分泌过多而导致AOM后ET功能的恶化,从而易患、维持或加重中耳疾病。(C)2003爱思唯尔爱尔兰有限公司。保留所有权利。
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 SIR 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. (C) 2003 Elsevier Ireland Ltd. All rights reserved.