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

Abstract
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.
AuthorsRobert J Homer, Tao Zheng, Geoff Chupp, Susan He, Zhou Zhu, Quingshen Chen, Bing Ma, R Duncan Hite, Laurice I Gobran, Seamus A Rooney, Jack A Elias
JournalAmerican journal of physiology. Lung cellular and molecular physiology (Am J Physiol Lung Cell Mol Physiol) Vol. 283 Issue 1 Pg. L52-9 (Jul 2002) ISSN: 1040-0605 [Print] United States
PMID12060560 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Interleukin-13
  • Proteolipids
  • Pulmonary Surfactant-Associated Protein A
  • Pulmonary Surfactant-Associated Proteins
  • Pulmonary Surfactants
  • RNA, Messenger
Topics
  • Animals
  • Asthma (immunology, pathology)
  • Bronchoalveolar Lavage Fluid (immunology)
  • Gene Expression (immunology)
  • Hypertrophy
  • Immunohistochemistry
  • Interleukin-13 (genetics)
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred CBA
  • Mice, Transgenic
  • Proteolipids (analysis, genetics)
  • Pulmonary Alveoli (chemistry, immunology, pathology)
  • Pulmonary Fibrosis (immunology, pathology)
  • Pulmonary Surfactant-Associated Protein A
  • Pulmonary Surfactant-Associated Proteins
  • Pulmonary Surfactants (analysis, genetics)
  • RNA, Messenger (analysis)

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