NUCLEAR FACTOR K B AND EOSINOPHILS IN ASTHMA PATHOGENESIS

Abstract

Asthma is a complex immunologic and inflammatory disease characterised by the presence of airway inflammation, airway remodelling, and bronchial huperresponsiveness (BHR). Eosinophils are circulating granulocytes involved in pathogenesis of asthma. Multiple elements including interleukin (IL)-5, IL-13, chemoattractants are directly involved in recruiting eosinophils to the lung during allergic inflammation. Once recruited, eosinophils participate in the modulation of immune response, induction of airway hyperresponsiveness and remodeling, characteristic features of asthma. Airwy eosinophilia has been recognized as a predominant feature of allergic asthma and elevated numbers during the inflammation are often associated with the disease severity. Increased eosinophil survival and decreased apoptotic death are believed to participate in the asthmaticc airways. The nuclear factor NF-κB pathway has long been considered a prototypical proinflammatory signaling pathway, largely based on the role of NF-κB in the expression of proinflammatory genes including cytokines, chemokines, and adhesion molecules. The NF-κB pathway does indeed regulate proinflammatory cytokine production, leukocyte recruitment, or cell survival, which are important contributors to the inflammatory response. But, the antiapoptotic functions of NF-κB can both protect against inflammation, in the case of epithelial cell survival and mucosal barrier integrity, and also maintain the inflammatory response through persistent leukocyte activation.