Open AccessCirculating intercellular adhesion molecule‐1 (ICAM‐1) antigen in sera of patients with idiopathic pulmonary fibrosis
Author(s) -
SHIJUBO N.,
IMAI K.,
AOKI S.,
HIRASAWA M.,
SUGAWARA H.,
KOBA H.,
TSUJISAKI M.,
SUGIYAMA T.,
HINODA Y.,
YACHI A.,
ASAKAWA M.,
SUZUKI A.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb06877.x
Subject(s) - intercellular adhesion molecule 1 , immunology , antigen , icam 1 , medicine , fibrosis , intercellular adhesion molecule , adhesion , idiopathic pulmonary fibrosis , intracellular , cell adhesion molecule , pathology , biology , lung , chemistry , cell adhesion , microbiology and biotechnology , organic chemistry
SUMMARY Intercellular adhesion molecule‐1 (ICAM‐1), a member of immunoglobulin supergene family with a five‐domain structure, is known to play an important role in inflammatory diseases. An ELISA was developed using two MoAbs against human ICAM‐1 in order to detect the soluble shedding ICAM‐1 antigen in sera. We measured levels of circulating ICAM‐1 antigen in sera of patients with idiopathic pulmonary fibrosis (IPF), pulmonary sarcoidosis, hypersensitive pneumonitis, bacterial and mycoplasmal pneumonia, and inflammatory diseases of other organs. The results clearly demonstrated that IPF had significantly high levels of circulating ICAM‐1 in sera as compared with other disorders or normal controls. Moreover, immunohistochemical analysis with MoAb against human ICAM‐1 disclosed that in IPF, the expression of ICAM‐1 was intensively enhanced on alveolar epithelial cells. These results suggest that ICAM‐1 may contribute to the pathogenesis of IPF.