The role of chemokines and cytokines in lung fibrosis

Idiopathic pulmonary fibrosis (IPF) exhibits a complex and poorly understood pathogenesis. Overt inflammation in the lungs of patients with established IPF is absent, and classic anti-inflammatory therapies are inefficacious; however, inflammation may contribute to the disruption of the normal alveolar architecture, allowing interaction between fibroblasts and the epithelium. The polarisation of the inflammatory response toward a type-2 helper T-cell phenotype may also be important in the development of pulmonary fibrosis, as fibroproliferation could be favoured over repair. Furthermore, evidence has emerged regarding an imbalance between angiogenic and angiostatic chemokine levels, leading to an overall angiogenic pattern of expression in both animal models and tissue specimens from IPF patients. The precise role of vascular remodelling in IPF remains to be determined. Therefore, numerous questions exist regarding the role and importance of chemokines and cytokines in pulmonary fibrosis. Further investigation is required to facilitate the elucidation of IPF pathogenesis and identification of novel targets for treatment of this dismal disease.