Role of ICAM-1 in the aggregation and adhesion of human alveolar macrophages in response to TNF-a and INF-g
Mediators of Inflammation(2014)
Abstract
CA Corresponding Author Tel: +81 18 884 6107 Fax: +81 18 836 2612 E-mail: masahiro@im2.med.akita-u.ac.jp IN TRAC ELLUL AR adhesion molecule-1 (ICAM-1)-mediated cellÐcell adhesion is thought to play an important role at sites of inflammation. Recent evidence suggests that ICAM-1 surface expression on alveolar macrophages is increased in pulmonary sarcoidosis and that inflammatory granuloma formation is characterized by the aggregation of macrophages. The present study shows that ICAM-1 expression is significantly elevated on alveolar macrophages from patients with sarcoidosis in response to tumor necrosis factora (TNFa ) and interferon-g (INFg ) compared with healthy controls. Aggregation and adhesion were significantly increased in alveolar macrophages treated with TNFa and INFg , and significantly inhibited in those pretreated with a monoclonal antibody to ICAM-1. Similarly, aggregation and adhesion were inhibited in macrophages treated with heparin, which then exhibited a wide range of biological activities relevant to inflammation. These results suggested that the surface expression of ICAM-1 on alveolar macrophages in response to TNFa and INFg is important in mediating aggregation and adhesion. Additionally, heparin may be useful for developing novel therapeutic agents for fibrotic lung disease.
MoreTranslated text
Key words
ICAM-1,alveolar macrophage,TNF-alpha,INF-gamma,sarcoidosis
AI Read Science
Must-Reading Tree
Example
![](https://originalfileserver.aminer.cn/sys/aminer/pubs/mrt_preview.jpeg)
Generate MRT to find the research sequence of this paper
Chat Paper
Summary is being generated by the instructions you defined