Background aims. Cirrhosis, end-stage liver disease, is caused by different mechanisms of injury, associated with persistent infl ammation. Galectin-3 is an important regulator of fi brosis that links chronic infl ammation to fi brogenesis. We investigated the role of bone marrow cell (BMC) transplantation in chronic infl ammation and hepatic fi brosis. Methods . Liver cirrhosis was induced by administration of carbon tetrachloride and ethanol to wild-type C57BL/6 or bone marrow chimeric mice. Bone marrow chimeras were generated by lethal irradiation and transplantation with BMC obtained from green fl uorescent protein (GFP )donors. Wild-type cirrhotic mice were transplanted with BMC without irradiation. Livers from chimeras and cirrhotic transplanted mice were obtained for evaluation of infl ammation, fi brosis and regulatory factors [galectin-3, matrix metallopeptidase (MMP)-9, tissue inhibitor of metalloproteinase (TIMP)-1 and transforming growth factor (TGF)- β ]. Results . The development of cirrhosis was associated with increased expression of galectin-3 by F4/80 cells and intense migration of BMC to the liver. Furthermore, when transplanted after the establishment of cirrhosis, BMC also migrated to the liver and localized within the fi brous septa. Two months after BMC therapy, cirrhotic mice had a signifi cant reduction in liver fi brosis and expression of type I collagen. We did not fi nd any difference in levels of TGF- β , TIMP-1 and MMP-9 between saline and BMC groups. However, the numbers of infl ammatory cells, phagocytes and galectin-3 cells were markedly lower in the livers of cirrhotic mice treated with BMC. Conclusions . Our results demonstrate an important role for BMC in the regulation of liver fi brosis and that transplantation of BMC can accelerate fi brosis regression through modulatory mechanisms