Fibrocytes are circulating mesenchymal precursors (CD45+, col 1+) recruited to 
fibrotic areas. Fibrocytes secrete profibrotic mediators including periostin; a 
matricellular protein that regulates cellular interactions with extracellular 
matrix (ECM) components. In bleomycin-induced fibrosis, periostin deficiency in 
structural or hematopoietic cells limits development of pulmonary fibrosis. To 
determine if hematopoietic-derived fibrocytes might secrete soluble factors to 
activate structural myofibroblast differentiation, wild-type (WT) fibroblasts 
were treated with conditioned medium from fibrocytes isolated from 
bleomycin-treated WT or periostin-/- mice. After 24 h we saw less α-smooth 
muscle actin expression in cells treated with conditioned medium from 
periostin-/- fibrocytes. Adoptive transfer of WT fibrocytes augmented lung 
fibrosis to a greater extent than transfer of fibrocytes from periostin-/- mice. 
In vitro analysis of fibrocytes and fibroblasts isolated from WT and 
periostin-/- mice treated with TGFβ1 or periostin demonstrated co-regulation of 
mesenchymal activation and beta 1 integrin as a potential receptor for periostin 
on fibrocytes. Additionally, connective tissue growth factor (CTGF) mRNA 
expression was increased in fibrocytes treated with periostin whereas CTGF and 
lysl oxidase (LOX) mRNA expression was low in bleomycin-treated periostin-/- 
fibrocytes. These data suggest fibrocytes may augment bleomycin-induced fibrosis 
via secretion of periostin and other soluble factors that promote myofibroblast 
differentiation.