Albino A P, Reed J A, Bogdany J K, Sassoon J, Parisier S C
Department of Otolaryngology, Manhattan Eye, Ear, & Throat Hospital, New York, New York 10021, USA.
Am J Otol. 1998 May;19(3):266-72.
Because many of the biologic phenomena in which mast cells are involved also are observed in human cholesteatoma pathology, the authors hypothesized that mast cells may play a role in this disease. The first test of this hypothesis is to determine whether there are an increased number of mast cells associated with cholesteatomas.
The molecular and cellular defects that result in the pathologic features observed in acquired and congenital cholesteatomas are unknown. One common feature of cholesteatoma pathogenesis is the presence of bacteria and a numerous inflammatory cytokines expressed by host inflammatory cells. The interactions between inflammatory cells and cholesteatoma epithelium could result in the induction of other aberrant biologic features of cholesteatomas. Thus, it is critical to the understanding of the pathogenesis of cholesteatomas to define the specific role of each cell type involved in this disease. Connective tissue mast cells have a complex retinue of functions mediated via the secretion of a variety of cytokines and proteinases, and many of the biologic phenomena in which mast cells are involved also are observed in cholesteatoma pathology.
The authors evaluated by immunohistochemistry 36 cholesteatomas of all types (e.g., primary and secondary acquired, recurrent, and congenital) and 23 specimens of normal tissues (e.g., tympanic membrane, canal wall skin, and postauricular skin) for the expression of tryptase, a mast cell-specific protease.
Cholesteatomas showed approximately threefold to sevenfold increase in the concentration of mast cells when compared with that of normal tissues. In addition, 19-34% of the mast cells were found within the suprabasal layers of the squamous epithelium of cholesteatoma subgroups, a phenomenon observed only in grossly inflamed tympanic membrane specimens, but not in other control tissues including minimally inflamed tympanic membranes.
The authors conclude from these data that mast cells may represent a previously unrecognized host inflammatory cell, which plays an important role in the development of one or more traits of cholesteatoma pathology.
由于肥大细胞所涉及的许多生物学现象也见于人类胆脂瘤病理学，作者推测肥大细胞可能在这种疾病中起作用。对这一假说的首次检验是确定与胆脂瘤相关的肥大细胞数量是否增加。
导致后天性和先天性胆脂瘤病理特征的分子和细胞缺陷尚不清楚。胆脂瘤发病机制的一个共同特征是细菌的存在以及宿主炎症细胞表达的多种炎性细胞因子。炎症细胞与胆脂瘤上皮之间的相互作用可能导致胆脂瘤其他异常生物学特征的诱导。因此，明确参与该疾病的每种细胞类型的具体作用对于理解胆脂瘤的发病机制至关重要。结缔组织肥大细胞具有通过分泌多种细胞因子和蛋白酶介导的复杂功能，并且肥大细胞所涉及的许多生物学现象也见于胆脂瘤病理学。
作者通过免疫组织化学评估了36例各种类型的胆脂瘤（如原发性和继发性后天性、复发性和先天性）以及23例正常组织标本（如鼓膜、外耳道壁皮肤和耳后皮肤）中肥大细胞特异性蛋白酶类胰蛋白酶的表达。
与正常组织相比，胆脂瘤中肥大细胞浓度显示出约三到七倍的增加。此外，在胆脂瘤亚组鳞状上皮的基底上层中发现19% - 34%的肥大细胞，这种现象仅在严重发炎的鼓膜标本中观察到，而在包括轻度发炎鼓膜在内的其他对照组织中未观察到。
作者从这些数据得出结论，肥大细胞可能代表一种先前未被认识的宿主炎症细胞，在胆脂瘤病理学一个或多个特征的发展中起重要作用。
