Alteration of the Expression of A 2 a Adenosine Receptor and Toll-like Receptor 4 in Macrophage Cell Lines

Abstract

Macrophages are essential for controlling the majority of infections, and are mediators of natural immunity. During an infection, lipopolysaccharide (LPS) stimulates macrophages to produce proinflammatory cytokines. Recently, it has been shown that A 2 a adenosine receptor (A 2 aR) is a critical part of the physiological negative feedback mechanism for the limitation and termination of tissue-specific and systemic inflammatory responses. It was useful and meaningful to gain information about interaction between LPS, which generates the inflammation, and adenosine receptors, which terminate the inflammation. However, very little, if anything, is known about the effect of bacterial LPS on the expression of A 2 aR during an infection of bacteria. The aim of this study is to evaluate the effects of adenosine, ATP and LPS on the expression of A 2 aR and toll-like receptor 4 (TLR 4), which is a receptor for LPS, in the mouse macrophage cell line RAW 264. Adenosine and ATP failed to affect proliferation in RAW 264 cells, whereas LPS increased proliferation. Adenosine significantly potentiated the expression of TLR 4, but not of A 2 aR. ATP and LPS markedly potentiated the expression of A 2 aR and TLR 4, respectively. Moreover, adenosine and ATP did not affect the expression of A 2 aR and TLR 4 in the presence of LPS, respectively. This study revealed that adenosine, ATP and LPS affect the expression of A 2 aR and TLR 4 in macrophages.