Pulmonary type II cell hypertrophy and pulmonary lipoproteinosis are features of chronic IL-13 exposure

Robert J. Homer, Tao Zheng, Geoff Chupp, Susan He, Zhou Zhu, Quingshen Chen, Ma Bing, R. Duncan Hite, Laurice I. Gobran, Seamus A. Rooney, Jack A. Elias

Research output: Contribution to journalArticlepeer-review


Interleukin (IL)-13, a key mediator of Th2-mediated immunity, contributes to the pathogenesis of asthma and other pulmonary diseases via its ability to generate fibrosis, mucus metaplasia, eosinophilic inflammation, and airway hyperresponsiveness. In these studies, we compared surfactant accumulation in wild-type mice and mice in which IL-13 was overexpressed in the lung. When compared with littermate controls, transgenic animals showed alveolar type II cell hypertrophy under light and electron microscopy. Over time, their alveoli also filled with surfactant in a pulmonary alveolar proteinosis pattern. At the same time, prominent interstitial fibrosis occurs. Bronchoalveolar lavage fluid from these mice had a three- to sixfold increase in surfactant phospholipids. Surfactant proteins (SP)-A, -B, and -C showed two- to threefold increases, whereas SP-D increased 70-fold. These results indicate that IL-13 is a potent stimulator of surfactant phospholipid and surfactant accumulation in the lung. IL-13 may therefore play a central role in the broad range of chronic pulmonary conditions in which fibrosis, type II cell hypertrophy, and surfactant accumulation occur.

Original languageEnglish (US)
Pages (from-to)L52-L59
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number1 27-1
StatePublished - 2002
Externally publishedYes


  • Asthma
  • Interleukin-13
  • Pulmonary fibrosis
  • Type 2 pneumocytes

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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