Monocyte-mediated mechanisms in idiopathic pulmonary fibrosis: opportunities for early intervention

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease marked by irreversible deposition of the extracellular matrix (ECM) and subsequent disruption of pulmonary architecture. Although current pharmacological interventions, such as Pirfenidone and Nintedanib, are available, they merely decelerate the progression of the disease. Notably, the monocyte count in peripheral blood is strongly correlated with the prognosis and mortality associated with IPF. An elevated monocyte count is observable in the early stages of IPF, with monocyte accumulation in lung tissue persisting throughout the disease's progression. Monocytes are recruited to the lung tissue in response to chemoattractant signals, where they differentiate into macrophages, dendritic cells, and fibrocytes. These differentiated cells are integral to the pathology of IPF, with macrophages, in particular, being identified as pivotal contributors to disease progression. This review aims to elucidate the primary pathways involved in monocyte recruitment to the lungs during IPF and to investigate the crucial roles that monocytes play in the disease's pathogenesis. This review aims to establish a foundation for novel therapeutic strategies targeting monocytes, thereby facilitating early detection and intervention in IPF.

Keywords: Chemokines; Extracellular matrix; Idiopathic pulmonary fibrosis; Macrophages; Monocytes.