In Vitro Data Supporting p38 MAPK Activation in Pulmonary Disease
The infiltration of the lungs by eosinophils is a prominent feature of asthma. These bone marrow-derived granulocytes can promote airway remodeling and tissue damage through the release of cytotoxic proteins and oxygen radicals (Giembycz and Lindsay 1999). The differentiation, recruitment, and activation of these cells result from the activity of an array of cytokines and chemokines including IL-3, IL-5, and eotaxin. Data generated using the p38 MAPK inhibitor SB 202190 demonstrated an inhibitory effect upon eosino-phil differentiation, degranulation, and cytokine release, suggesting a role for this pathway in eosinophil effector functions (Adachi et al. 2000). Changes in airway osmolarity have been hypothesized to contribute to exercise-induced bronchoconstriction and the late-phase airway response. Exposure of bronchial epithelial cells to hyperosmolar medium has been shown to induce expression of the neutrophil chemoattractant chemokine IL-8, which is inhibited by SB 203580 (Shapiro and Dinarello 1995; Matsumoto et al. 1998; Hashimoto et al. 1999).
Was this article helpful?
If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.