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Gene transfer for cytokine functional studies in the lung: the multifunctional role of GM‐CSF in pulmonary inflammation
Author(s) -
Xing Zhou,
Braciak Todd,
Ohkawar Yuichi,
Sallenave JeanMichel,
Foley Ronan,
Sime Patricia J.,
Jordana Manel,
Graham Frank L.,
Gauldie Jack
Publication year - 1996
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.59.4.481
Subject(s) - biology , immunology , proinflammatory cytokine , cytokine , inflammation , granulocyte macrophage colony stimulating factor , macrophage , lung , macrophage inflammatory protein , eosinophilia , alveolar macrophage , interleukin , medicine , biochemistry , in vitro
Using adenoviral‐mediated gene transfer techniques, the murine granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) transgene is efficiently targeted to and highly expressed by the respiratory epithelium of rat lung. This lung tissue‐directed expression of GM‐CSF induces accumulation of both eosinophils and macrophages at early stages and an irreversible fibrotic reaction at later stages. These tissue responses to GM‐CSF appear to be distinct from those induced by other proinflammatory cytokines, interleukin (IL) ‐5, IL‐6, macrophage inflammatory protein‐2 (MIP‐2), or RANTES overexpressed in the lung. These findings clearly demonstrate that GM‐CSF is more than a hematopoietic cytokine in the lung and may play a pivotal role in the multiple pathological processes underlying numerous respiratory illnesses, including asthma. In this overview, the differences in tissue responses induced by GM‐CSF and other individual cytokines are highlighted. In addition, the mechanisms by which GM‐CSF contributes to the development of eosinophilia, macrophage granuloma, and fibrosis are discussed in conjunction with the recent findings from us and others.