Bronchial mucosal inflammation

Asthma is a chronic inflammatory condition characterized by bronchial hyper-responsiveness and reversible airway obstruction. Cytokine release from a variety of cell types such as eosinophils, lymphocytes and other inflammatory cells produces epithelial sloughing, plasma protein extravasation from the tracheobronchial microcirculation and airway remodeling. Bronchial mucosal inflammation is present in all patients. The primary goal of asthma management is to maintain control of the disease process by reducing symptoms and improving lung function. 

Thus, we demonstrated here in vivo that mucosal contact with SEB is capable of aggravating several features of bronchial allergic inflammation bronchial eosinophilic inflammation, IL-4, IL-5 and IFN-y levels in bronchi and systemic circulation, bronchial expression of eotaxin-1 and TGF-(3, and allergen-specific IgE titers [53], Not only bronchial but also nasal mucosal contact with SEB is capable of inducing a more severe bronchial allergic inflammation in sensitized mice. 

Exposure of rats to 800 ppm for 15 minutes was fatal, but nearly all survived when exposed for 13 minutes. There was severe inflammation of all exposed mucosal surfaces, resulting in lacrimation, corneal ulceration, and burning of exposed areas of skin. In another study, exposure of rats to 480 ppm for 40 minutes or to 96ppm for 3.7 hours was fatal in the latter group, effects were pulmonary edema and marked irritation of the bronchial mucosa. Chronic exposure of dogs and rats to about Ippm, 6 hours/day for up to 6 months caused severe pulmonary irritation and some deaths. ... 

Many corticosteroids undergo metabolism via CYP3A4 and are substrates of P-gp. They are used to suppress inflammation in the respiratory tract, reducing mucosal oedema and decreasing bronchial secretions. They are employed both to prevent acute exacerbations of chronic airways disease and to treat acute flare-ups. They may be subject to interactions when administered orally, but interactions with high-dose inhaled formulations are thought to occur due to steroid that is deposited in the oropharynx, swallowed and absorbed via the gastrointestinal tract. 

The biological actions of capsaicin are primarily attributable to release of the neuropeptide substance P, calcitonin gene-related peptide (CGRP), and neurokinin A from sensory neurons. These transmitters from primary sensory neurons communicate witir other cell types. They produce alterations in the airway mucosa and neurogenic inflammation of the respiratory epithelium, airway blood vessels, glands, and smooth muscle. Alterations in multiple effector organs lead to bronchoconstriction, increased vascular permeability, edema of the tracheobronchial mucosa, elevated mucosal secretion, and neutrophil chemotaxis (Tominack and Spyker, 1987). Capsaicin-induced effects of bronchoconstriction, vasodilation, and plasma protein extravasation are mediated by substance P. In addition, substance P can cause bronchoconstriction through stimulation of c-fibers in pulmonary and bronchial circulation. 

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