Alveolar type II cells transplantation decrease fibrocyte migration in pulmonary fibrosis

Póster presentado en el 23rd Annual Congress European Respiratory Society (ERS) celebrado del 7 al 11 de septiembre de 2013 en Barcelona (España)Abstract publicado en "European Respiratory Journal" 42 (Suppl 57): 115s (2013)One of the most important features of the pathogenesis of pulmonary fibrosis is epithelial cell injury and fibroblast proliferation. The original source of this aberrant fibroblast overpopulation might proceed from the lung resident fibroblasts, or could come from circulating fibrocytes migration and its subsequent differentiation to fibroblasts/myofibroblasts. In a previous study our group demonstrated that intratraqueal transplantation of alveolar type II cells (ATII) can reverse the fibrotic process in a rat model of bleomycin-induced lung fibrosis. The objective of this study was to determine whether ATII transplant was able to inhibit fibrocyte recruitment into the fibrotic lung. Lung fibrosis was induced by intratraqueal instillation of bleomycin (3.5U/kg). The animals were transplanted with ATII (2.5x106 cells/animal) 15 days after bleomycin instillation and were sacrificed 21 days after the induction of fibrosis. The expression of CXCL12/CXR4 axis, involved in the recruitment of fibrocytes, was assessed by real time RT-PCR in peripheral blood, lung tissue and isolated cells (macrophages and fibroblasts). Protein synthesis was analyzed by immunohistochemistry in tissue slices. Fibrotic animals showed increased expression of CXCR4 in both peripheral blood and lung tissue. ATII transplantation was able to significantly reduce these increments. Furthermore, although fibrotic animals also showed increases in CXCL12 expression in pulmonary macrophages, these increases were inhibited in the fibrotic transplanted animals. In conclusion ATII transplantation is able to inhibit the fibrocyte recruitment reducing the fibrocyte infiltration to lung tissue and then stopping fibrosisPeer Reviewe