Brazís P, Queralt M, de Mora F, Ferrer L, Puigdemont A
Departament de Farmacologia, Facultat de Veterinària, Universitat Autònoma de Barcelona, Spain.
Vet Immunol Immunopathol. 1998 Nov 6;66(1):43-51. doi: 10.1016/s0165-2427(98)00193-7.
Atopic dermatitis results from the interaction between allergen and allergen-specific IgE bound to the mast cell surface receptors. This process triggers mast cell degranulation and accounts at least for early phase reaction. Furthermore, there is increasing in vitro and in vivo evidence that IgE has the ability to induce overexpression of the Fc epsilonRI receptor on the mast cell plasma membrane. In order to study the potential effect of an increase in serum IgE on mast cell activity, the histamine releasability of mature mast cells isolated from the skin of atopic, ascaris-sensitive and healthy dogs was analyzed. No histamine release was detected upon the immunological stimulation of cells that were not previously sensitized with atopic or ascaris-sensitive dog serum. However, when passively sensitized, skin mast cells were challenged with either Asc SI antigen or anti-IgE, the mast cell histamine release increased in a stimulus concentration-dependent manner. The amount of histamine released was significantly higher in response to anti-IgE than in response to Asc SI antigen. However. the difference in the percentage of mast cell histamine release between atopic (26.3+/-2.8%) and non-atopic (30.9+/-1.7%) dogs was not statistically significant, similar to what occurred when ascaris-sensitive (12.8+/-1.6%) and non-sensitive (13.2+/-1.7%) dogs were compared. Although these results could suggest that there is either little or no increase in the density of IgE receptors in atopic or ascaris-hypersensitive dogs versus controls, we strongly consider either the possibility that the digestion procedure might affect cell behaviour in vitro or that an underlying increase of receptors poorly affects the release of granule-stored mediators but influences mast cell activity in a different manner.
特应性皮炎是由变应原与结合在肥大细胞表面受体上的变应原特异性IgE之间的相互作用引起的。这一过程触发肥大细胞脱颗粒，至少是早期反应的原因。此外，越来越多的体外和体内证据表明，IgE有能力诱导肥大细胞质膜上FcεRI受体的过度表达。为了研究血清IgE增加对肥大细胞活性的潜在影响，分析了从特应性、蛔虫敏感和健康犬皮肤中分离出的成熟肥大细胞的组胺释放能力。对未预先用特应性或蛔虫敏感犬血清致敏的细胞进行免疫刺激时，未检测到组胺释放。然而，当被动致敏的皮肤肥大细胞用Asc SI抗原或抗IgE攻击时，肥大细胞组胺释放以刺激浓度依赖的方式增加。抗IgE刺激后释放的组胺量明显高于Asc SI抗原刺激后释放的组胺量。然而，特应性犬（26.3±2.8%）和非特应性犬（30.9±1.7%）之间肥大细胞组胺释放百分比的差异无统计学意义，蛔虫敏感犬（12.8±1.6%）和非敏感犬（13.2±1.7%）比较时也是如此。尽管这些结果可能表明，与对照组相比，特应性或蛔虫过敏犬的IgE受体密度几乎没有增加或没有增加，但我们强烈认为，要么消化程序可能影响体外细胞行为，要么受体的潜在增加对颗粒储存介质的释放影响不大，但以不同方式影响肥大细胞活性。
