Pediatric Respiratory Diseases by Unknown

Author:Unknown
Language: eng
Format: epub
ISBN: 9783030269616
Publisher: Springer International Publishing

Etiopathogenesis

The inflammation of the airway is the result of the interaction of different effector cells and proinflammatory mediators. In patients with atopic asthma, the predominance of type Th2 lymphocytes produces a proinflammatory state, with the participation of dendritic neuronal cells and release of cytokines such as interleukin (IL)-3, IL-4, IL-5, and IL-10, which affect local cells, including epithelial cells, but also affect recruited cells, such as eosinophils. Other cells, such as macrophages and mastocytes, interact to boost this permanent state of inflammation. The release of second mediators such as leukotrienes, histamines, and prostaglandins produces the most common epithelial alterations of a patient with asthma, such as bronchoconstriction, hypersecretion, and epithelium disruption. In a preferably eosinophilic inflammation environment, the enlargement of the reticular layer in the basal lamina, and hyperplasia of mucosal glands as well as smooth muscle and vascular tissues, increase the width of the bronchus wall, which makes the bronchi more rigid and reduces the transversal section of the airway: this causes a reduction of pulmonary function and a greater unspecific BHR. These changes in the airway structure would be responsible for the most serious presentation of the disease and of its chronic condition. These mechanisms explain that the disease may be reversible when treated, or it will only be partially reversible because of the damage caused. Therefore, there are multiple mediators involved in promoting the inflammation and obstruction of the airway, although their relative importance is difficult to determine (Fig. 41.1).

Fig. 41.1Inflammation physiopathology

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