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.