Interleukin-11 disrupts alveolar epithelial progenitor function.

Background: Interleukin-11 (IL-11) is linked to the pathogenesis of idiopathic pulmonary fibrosis (IPF), since IL-11 induces myofibroblast differentiation and stimulates their excessive collagen deposition in the lung. In IPF there is disrupted alveolar structural architecture, yet the effect of IL-11 on the dysregulated alveolar repair remains to be elucidated.

Methods: We hypothesised that epithelial-fibroblast communication associated with lung repair is disrupted by IL-11.