Paracrine functions of fibrocytes to promote lung fibrosis

Abstract

Fibrocytes are derived from the bone marrow and are found in the circulation. They can be recruited to sites of injury and contribute to repair/remodeling. In vitro evidence suggests that fibrocytes may differentiate into fibroblasts to promote lung fibrosis. However, in vivo evidence for this is sparse. This review summarizes recent literature which may suggest that fibrocytes function to promote fibrosis via paracrine actions. In this way, secretion of growth factors, proteases and matricellular proteins may strongly influence the actions of resident epithelial and mesenchymal cells to promote repair and resolution or to tip the scale toward pathologic remodeling.

Figure 1

Proposed Paracrine Functions of Fibrocytes. Fibrocytes express a number of cell surface receptors which can regulate their recruitment and secretion of signaling factors. These factors can further regulate fibrocyte function and/or regulate the function of other cells in autocrine and paracrine fashion. Abbreviations: IL-R=interleukin receptor, GF-R=growth factor receptor, ECM=extracellular matrix, Col=collagen, FN=fibronectin, PO=periostin, CTGF=connective tissue growth factor, TGFβ=transforming growth factor β, PDGF=platelet derived growth factor, bFGF=basic fibroblast growth factor, cysLT= cysteinyl leukotrienes, IL1β=interleukin 1β, IL6=interleukin 6, MIP=macrophage inflammatory protein, CCL2=chemokine ligand 2.