As in RA, inflammatory cytokines play a crucial role in the pathogenesis of airways inflammation. Cytokines such as TNF, interferon (IFN)-g, IL-4, IL-5, and chemokines such as IL-8, regulated upon activation normal T cells expressed and secreted (RANTES) and eotaxin have all been demonstrated to be capable of generating or supporting airways inflammation (Barnes et al. 1998). The generation and signaling of many of these mediators has also been shown to be dependent on the MAPK cascade. It is therefore postulated that inhibition of p38a MAPK may have a beneficial effect in the treatment of pulmonary diseases including asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF).
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