ABSTRACT
The presence of a Th2-driven chronic inflammation of the lower airway mucosa is currently considered to be the central feature in the pathogenesis of asthma. This inflammatory process shows not only features characteristic of an acute inflammatory response such as vasodilatation, plasma exudation, or the presence of activated inflammatory cells but also characteristics of a more chronic phase of an inflammatory reaction that results in tissue remodeling (1). This inflammatory process is orchestrated and regulated by a complex network of mutually interacting cytokines and growth factors released not only from Th2 cells but from a wide range of inflammatory cells as well as structural tissue components. Tumor necrosis factor α (TNFα) and interleukin-1β (IL-1β) are among the cytokines that could play an important role within this network. Several studies have demonstrated increased amounts of TNFα and IL-1β at either the mRNA or protein level in sputum (2,3), BAL (4-6), or biopsies from asthmatic patients (7-10). Hence the interest in inhibitors of the these cytokines as a potential novel form of asthma treatment.
