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The pathogenesis of asthma is not entirely clear. Most people believe that allergy, chronic airway inflammation, increased airway responsiveness and [4] autonomic dysfunction and other factors interact to participate in the pathogenesis of asthma.
(A) allergic reaction when allergens enter the body with allergies, the adoption of macrophages and T lymphocytes of the transmission, can stimulate the body's synthesis of B-lymphocyte-specific IgE, in combination with mast cells and basophils in the cell surface high-affinity IgE receptor (FcεR1). If the allergen re-entered the body, with mast cells and basophils surface IgE cross-linking, thereby precipitating a series of reactions within cells, so that the cells produce and release a variety of active media, leading to smooth muscle contraction, mucus secretion increased , vascular permeability and inflammatory cell infiltration. Inflammatory cells under the influence of the medium can also secrete a variety of media, so that increased airway disease, inflammatory infiltration increased, resulting in clinical symptoms of asthma.
According to asthma after allergen inhalation time can be divided into rapid onset asthmatic reaction (IAR), late-onset asthmatic reaction (LAR) and bipolar-type asthmatic reaction (OAR). IAR almost immediately, while inhaled allergens react with 15 to 30 minutes and reached the peak, 2 hours after gradually returning to normal, belongs to type Ⅰ allergy. LAR about 6 hours onset, lasted longer, up to several days. And the clinical symptoms of weight, Changcheng the performance of persistent asthma, lung function damage to severe and prolonged. The pathogenesis of LAR more complex, not only with IgE-mediated mast cell degranulation and were mainly caused by airway inflammation. Asthma is now considered a variety of inflammatory cells involved in the interaction of many mediators and cytokines involved in a chronic airway inflammatory diseases. LAR primary and airway inflammation.
(B) chronic airway inflammation and airway inflammation in asthma is considered the basic pathological changes and recurrent major pathophysiological mechanisms. No matter what type of asthma, which phase of asthma, have demonstrated for the in mast cells, eosinophils and T lymphocytes mainly of a variety of inflammatory cells in the airway infiltration and aggregation. Interaction between these cells can secrete dozens of inflammatory mediators and cytokines. These media, cytokines and inflammatory cells in a complex network of interactions, interaction and influence, so that airway inflammation persists. When the body triggers encountered, these inflammatory cells to release a variety of inflammatory mediators and cytokines, causing airway smooth muscle contraction, mucus secretion, plasma exudation and mucosal edema. Known to a variety of cells, including mast cells, eosinophils, neutrophils, epithelial cells, macrophages and endothelial cells can produce inflammatory mediators. The main media are: histamine, prostaglandin (PG), leukotrienes (LT), platelet-activating factor (PAF), eosinophil chemotactic factor (ECF-A), neutrophil chemotactic factor ( NCF-A), major basic protein (MBP), eosinophil cationic protein (ECP), endothelin -1 (ET-1), adhesion molecules (adhesion molecules, AMs) and so on. In summary, chronic airway inflammation in asthma is caused by various inflammatory cells, inflammatory mediators and cytokines involved, the interaction of a vicious circle, so that airway inflammation persists. Their mutual relations are very complex and needs further research.
(C) airway hyperresponsiveness (AHR) showed a variety of stimulating factors of airway appear too strong or premature contraction response is the development of asthma patients in another important factor. Now widely recognized that airway inflammation leading to airway hyperresponsiveness, one of the important mechanisms. Airway epithelial damage and epithelial nerves in the regulation of such factors are also involved in the pathogenesis of AHR. When the airway by allergen or other stimulus, due to a variety of inflammatory cells to release inflammatory mediators and cytokines, so that the parasympathetic nerve axon reflex excitability increase in neuropeptide release, are related to the process with the pathogenesis of AHR. Road, in patients with bronchial asthma, AHR is a common pathophysiological features, but there were not all bronchial asthma, AHR, such as the long-term smoking, ozone exposure, viral upper respiratory tract infection, chronic obstructive pulmonary disease (COPD), also can occur AHR. From the clinical point of view, a very mild AHR needed to diagnose with clinical manifestations. But more than moderate AHR almost certainly asthma.
(D) The neural mechanisms underlying neural factors are also considered to be an important part of asthma. Bronchus by the complex autonomic control. In addition to cholinergic, adrenergic nerves, there are non-adrenergic non-cholinergic (NANC) nervous system. Bronchial asthma with β-adrenergic receptor dysfunction and vagal hypertonia related, and may be the existence of α-adrenergic nerve responses increased. NANC relaxation of bronchial smooth muscle to the release of neurotransmitters such as vasoactive intestinal peptide stimulated (VIP), nitric oxide (NO), as well as contraction of bronchial smooth muscle of the media, such as substance P, neurokinin and so on. Imbalance between the two may cause bronchial smooth muscle contraction.

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