Aim: 

Bradykinin is an mediator that could play a pivotalrole in the pathogenesisof inflammation, tissue damage, and repair in chronic pulmonary inflammatory diseases, characterized by changes in airway responsiveness. Bradykinin elicits bronchoconstriction in most species and could be involved in asthma and certain lung fibrosis. In the present work, we demonstrate that bradykinin leads fibroblasts into a myofibroblast phenotype at the cellular and molecular level.

Methods: 

Flow cytometry and RT-PCR was used to detect the presence of alpha-Smooth Muscle Actin (a-SMA), a marker of myofibroblast, in human lung fibroblast cultures. Control cultures were compared with those in which bradykinin was added. Cell proliferation and collagen production were evaluated by the colorimetric methylthiazol tetrazolium assay and sirius red assay, respectively.

Results: 

Bradykinin caused in lung fibroblasts culture a significant increase in a-SMA. Bradykinin was able to induce fibroblast proliferation and collagen production.

Conclusion: 

These data demonstrate that bradykinin may be involved in bronchial remodeling and lung fibrosis beyond its well recognized proinflammatory activity.