Abstract
Recently, Laitinen and his co-workers [1] have demonstrated a significant increase in the number of mast cells (p < 0.001), lymphocytes, eosinophils and macrophages (p < 0.5) in the bronchial epithelium of patients with newly diagnosed asthma. Others also have observed a 5-to 6-fold increase in the percentage of mast cells in the bronchoalveolar lavage (BAL) fluid of mild atopic asthmatics as compared with that in the healthy subjects [2]. These observations demonstrate the presence of allergic airway inflammatory processes even at the very early stages of asthma. Mast cell activation and histamine secretion not only play a pivotal role in the initiation of allergic airway inflammation [3, 4] but may also sustain chronic inflammatory processes by upregulating self induction of interleukin (IL)-1β through histamine release [5], expression of adhesion molecules such as intercellular adhesion molecule (ICAM)-1 on the airway epithelium [6] and interactions with cytokines [7]. Mast cell activation resulting in histamine secretion, generation of cytokines and leukotrienes as well as subsequent release of neuropeptides and other mediators and their possible synergistic interactions may play an important role in the pathogenesis of acute as well as chronic allergic inflammatory processes such as rhinitis and asthma in the upper and lower airways [1–7].
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Chand, N., Sofia, R.D. (1995). Histamine. In: Raeburn, D., Giembycz, M.A. (eds) Airways Smooth Muscle: Neurotransmitters, Amines, Lipid Mediators and Signal Transduction. Respiratory Pharmacology and Pharmacotherapy. Birkhäuser Basel. https://doi.org/10.1007/978-3-0348-7504-2_3
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