Department of Microbiology and Immunology, Thomas Jefferson University, 223 South 10th Street, Bluemle Life Science Building Room 750, Philadelphia, PA 19107, USA.
Immunol Res. 2011 Dec;51(2-3):215-26. doi: 10.1007/s12026-011-8250-x.
In developed countries, the prevalence of allergy is on the rise. Although the causes are unknown, it seems that (1) the disappearance of microbiota may play a role in the increase of allergies and (2) exposure to bacterial infections during childhood decreases the incidence of allergies. Although several cell types are involved in the development of allergy, mast cells play a major role in orchestrating inflammation. Upon activation, mast cell secretory granules fuse with the plasma membrane, resulting in the release of a number of inflammatory mediators. In addition to allergy, mast cells contribute to the innate immune response against a variety of bacteria. This is accomplished through the secretion of cytokines and other soluble mediators. Interestingly, there is growing evidence that mast cells exposed to bacteria down-regulate degranulation in response to IgE/Allergen stimulation. This inhibitory effect seems to require direct contact between bacteria and mast cells, but the intracellular mechanism by which bacterial contact suppresses allergic responses is unknown. Here, we review different aspects of mast cell physiology and discuss hypotheses as to how bacteria may influence mast cell degranulation.
在发达国家,过敏的患病率呈上升趋势。尽管其病因尚不清楚,但(1)微生物组的消失似乎在过敏的增加中起作用,(2)儿童时期接触细菌感染会降低过敏的发生率。尽管有几种细胞类型参与了过敏的发生,但肥大细胞在炎症的调控中起着主要作用。肥大细胞活化后,其分泌颗粒与质膜融合,导致多种炎症介质的释放。除过敏外,肥大细胞还有助于针对各种细菌的先天免疫反应。这是通过细胞因子和其他可溶性介质的分泌来实现的。有趣的是,越来越多的证据表明,暴露于细菌的肥大细胞会下调对 IgE/变应原刺激的脱颗粒作用。这种抑制作用似乎需要细菌与肥大细胞之间的直接接触,但细菌接触抑制过敏反应的细胞内机制尚不清楚。在这里,我们综述了肥大细胞生理学的不同方面,并讨论了细菌可能影响肥大细胞脱颗粒的假说。