Abstract
Macrophages are essential for controlling the majority of infections, and are mediators of natural immunity. During infection, lipopolysaccharide (LPS) stimulates macrophages to produce pro-inflammatory cytokines. Interferon-γ (IFN-γ) is also a major activation factor for macrophages. More recently, it has been shown that A2a adenosine receptor (A2aR) is a critical part of the physiological negative feedback mechanism for limitation and termination of tissue-specific and systemic inflammatory responses. It is useful and meaningful to gain information about interaction with LPS, which generates the inflammation, and IFN-γ, which is a major activation factor for macrophages, and adenosine receptors, which terminate the inflammation. The aim of this study is to evaluate the abilities of adenosine, LPS and IFN-γ on the expression of A2aR in the mouse macrophage cell line RAW264.
Only LPS (10 ng/mL) increased the proliferation in RAW264. ATP (10-4 M) markedly potentiated the expression of A2aR in RAW264. Similarly IFN-γ (102 unit/mL and 103 unit/mL) significantly potentiated the expression of A2aR in RAW264.
These results suggest that ATP and IFN-γ may affect the expression of A2aR in macrophages.
