Understanding XXXX pathophysiology.

@entity1 @entity32 @entity2086 @entity12288 @entity1712 @entity404 @entity225 @entity2488 @entity4047 @entity565 @entity4 @entity4443 @entity102 @entity358 @entity1729 @entity112 @entity3646 @entity9416 @entity2710 @entity1224
@entity565 is best described as a @entity102 that involves @entity32 of the pulmonary airways and @entity2488 that results in the clinical expression of a lower @entity1224 that usually is reversible. Physiologically, @entity2488 is documented by decreased bronchial airflow after bronchoprovocation with @entity2710 or @entity112 . Other triggers that provoke @entity1224 include cold air, exercise, @entity1729 , cigarette smoke, and respiratory allergens. Bronchial provocation with allergen induces a prompt early phase @entity9416 ( @entity9416 )-mediated decrease in bronchial airflow (forced expiratory volume in 1 second) followed in many @entity1 by a late-phase @entity9416 -mediated reaction with a decrease in bronchial airflow for 4-8 hours. The gross pathology of @entity358 , smooth @entity2086 , @entity12288 thickening, @entity4 , epithelial cell sloughing, cilia cell disruption, and mucus gland hypersecretion. Microscopically, @entity565 is characterized by the presence of increased numbers of @entity1712 , neutrophils, lymphocytes, and plasma cells in the bronchial tissues, bronchial secretions, and mucus. Initially, there is recruitment of leukocytes from the bloodstream to the airway by activated @entity404 T-lymphocytes. The activated T-lymphocytes also direct the release of inflammatory mediators from @entity1712 , mast cells, and lymphocytes. In addition, the subclass 2 helper T-lymphocytes subset of activated T-lymphocytes produces interleukin (IL)-4, @entity225 , and @entity4047 . @entity3646 in conjunction with @entity4047 signals the switch from IgM to @entity9416 antibodies. The cross-linkage of two @entity9416 molecules by allergen causes mast cells to degranulate, releasing @entity112 , @entity4443 , and other mediators that perpetuate the airway @entity32 . @entity225 activates the recruitment and activation of @entity1712 . The activated mast cells and @entity1712 also generate their cytokines that help to perpetuate the @entity32 . Regardless of the triggers of @entity565 , the repeated cycles of @entity32 in the lungs with injury to the pulmonary tissues followed by repair may produce long-term structural changes ("remodeling") of the airways. This review will discuss in greater detail the relationships of @entity32 and airway hyperresponsiveness to the pathophysiology of @entity565 .
