Dynamics of innate immunity cytokines in patients with COPD

Chronic obstructive pulmonary disease (COPD) typically induces and maintains the activation of several phylogenetically old adaptative and defensive mechanisms. Activation is usually needed for a limited period during acute injury. In chronic disease conditions, however, those mechanisms are kept activated for longer periods. Eventually, irreversible damage is produced and this contributes to impaired function and worse prognosis in a variety of chronic diseases. The inflammatory cells and human bronchial smooth muscles are known to play an important role in the production of innate immunity cytokines and neurotrophins which have been recognized as mediators of both inflammatory and airway remodeling processes. When neurotrophins such as Neurotrophin 3 (NT-3) were initially discovered, they were thought to be only regulatory factors of the development, differentiation and survival of the neurons. Later, it was proved that they are also involved in inflammatory responses. In experimental animal models, neurotrophin may contribute to the development of bronchial hyperresponsivness. The persistent activation of the innate immune system by smoke exposure, releases the ROS that lead to a pronounced chronic inflammation of both airway and pulmonary parenchyma.