Perskvist N, Edston E
National Board of Forensic Medicine, Linköping Division, Department of Forensic Medicine, Artillerigatan 12, SE-58133 Linköping, Sweden.
Forensic Sci Int. 2007 Jun 14;169(1):43-9. doi: 10.1016/j.forsciint.2006.08.001. Epub 2006 Nov 1.
The distribution profile of infiltrated mast cell-subpopulations and eosinophils in the lung and heart sections of the patients who died of severe allergic hyperresponsiveness, was investigated. Four study groups were designed comprising 9 cases who died in systemic anaphylaxis (Group I), 10 asthmatic individuals whose death were assigned to acute and severe bronchial asthma (Group II), 10 asthmatic cases who died from non-immunological diseases (Group III). Twenty consecutive autopsies of non-allergic subjects who died of unnatural causes (Group IV) served as control group in this study. Utilizing antibodies against human tryptase and chymase and a double immunohistochemical staining method, we distinguished successfully all three subsets of mast cells (MC), MC-TC (containing both tryptase and chymase), MC-T (containing only tryptase) and MC-C (containing only chymase) types, subdivided on the basis of the protease compositions of their secretory granules. In order to immunostaining eosinophils, we used antibody to major basic protein as a marker. We also measured postmortem blood tryptase, specific and total serum IgE. The intriguing finding of this study was the marked differences of cellular composition in the lung between fatal anaphylaxis and asthma death. Significant augmentation of MCs infiltrated in lung and heart sections of anaphylaxis patients and drastic infiltration of bronchial eosinophils in asthmatic death and consequent release of their related inflammatory mediators might explain the differential expression of the associated symptoms in these two groups. The anaphylactic deaths did show neither emphysema nor significant mucous bronchial secretions whereas all asthmatic deaths did. The degree of pulmonary congestion and edema was also more severe in anaphylaxis. This corresponded with the histological findings and the location and number of mast cell-subsets and eosinophils in the different compartments of the lungs. We have demonstrated that the third type of mast cell MC-C is only found in the lungs in anaphylactic deaths. The practical consequence of our study will be that it is now possible to confirm a suspicion of anaphylaxis death not only by measurements of serum mast cell tryptase, but also by immunohistochemical methods.
对死于严重过敏反应过度的患者肺部和心脏切片中浸润的肥大细胞亚群和嗜酸性粒细胞的分布情况进行了研究。设计了四个研究组,包括9例死于全身性过敏反应的病例(第一组)、10例因急性重度支气管哮喘死亡的哮喘患者(第二组)、10例死于非免疫性疾病的哮喘病例(第三组)。连续20例死于非自然原因的非过敏受试者尸检(第四组)作为本研究的对照组。利用抗人组织蛋白酶和糜蛋白酶抗体以及双重免疫组织化学染色方法,我们成功区分了肥大细胞(MC)的所有三个亚群,即MC-TC(同时含有组织蛋白酶和糜蛋白酶)、MC-T(仅含组织蛋白酶)和MC-C(仅含糜蛋白酶)类型,这些亚群是根据其分泌颗粒的蛋白酶组成划分的。为了对嗜酸性粒细胞进行免疫染色,我们使用抗主要碱性蛋白抗体作为标记物。我们还测量了死后血液中的组织蛋白酶、特异性和总血清IgE。本研究的有趣发现是,致命性过敏反应和哮喘死亡患者肺部的细胞组成存在显著差异。过敏反应患者肺部和心脏切片中浸润的肥大细胞显著增加,哮喘死亡患者支气管中嗜酸性粒细胞大量浸润,以及随之释放的相关炎症介质,可能解释了这两组患者相关症状的不同表现。过敏反应死亡患者既没有肺气肿,也没有明显的支气管黏液分泌,而所有哮喘死亡患者都有。过敏反应患者肺部充血和水肿的程度也更严重。这与组织学结果以及肺部不同区域肥大细胞亚群和嗜酸性粒细胞的位置和数量相符。我们已经证明,第三种类型的肥大细胞MC-C仅在过敏反应死亡患者的肺部中发现。我们研究的实际意义在于,现在不仅可以通过测量血清肥大细胞组织蛋白酶,还可以通过免疫组织化学方法来证实对过敏反应死亡的怀疑。