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Lungs of patients with idiopathic pulmonary alveolar proteinosis express a factor which neutralizes granulocyte‐macrophage colony stimulating factor
Author(s) -
Tanaka Naohiko,
Watanabe Junichi,
Kitamura Takayuki,
Yamada Yoshitsugu,
Kanegasaki Shiro,
Nakata Koh
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01668-8
Subject(s) - pulmonary alveolar proteinosis , granulocyte , granulocyte macrophage colony stimulating factor , alveolar macrophage , macrophage , immunology , granulocyte macrophage colony stimulating factor receptor , granulocyte colony stimulating factor , medicine , lung , pathology , chemistry , cytokine , macrophage colony stimulating factor , in vitro , biochemistry , chemotherapy
Mice deficient in granulocyte‐macrophage colony stimulating factor (GM‐CSF) develop pulmonary alveolar proteinosis (PAP). We found that bronchoalveolar lavage fluid (BALF) from 11 patients with idiopathic pulmonary alveolar proteinosis (IPAP) suppressed the growth of peripheral blood monocytes and TF‐1 cells, a cell line dependent on either GM‐CSF or interleukin‐3 (IL‐3). The inhibitory effect of PAP‐BALF occurred only when TF‐1 cells were cultured with GM‐CSF but not when cultured with IL‐3, suggesting that PAP‐BALF contains a factor that specifically interferes with GM‐CSF function. 125 I‐GM‐CSF binding to TF‐1 cells was prevented in the presence of BALF from IPAP patients. Furthermore, cross‐linking of 125 I‐GM‐CSF to IPAP‐BALF produced two major bands on SDS‐PAGE; these bands were not observed in normal BALF. These data suggest that IPAP is caused by expression of binding factor(s) which inhibit GM‐CSF function in the lung.