Inflammation 'stop' button

The mechanisms that control the termination of the mammalian inflammatory response in vivo remain unclear. In 20/27 December Nature Akio Ohta & Michail Sitkovsky from National Institutes of Health, Bethesda, USA show that G-protein-coupled A2a adenosine receptors have an essential role in the attenuation of inflammation and tissue damage in vivo.

Ohta & Sitkovsky studied mice deficient in the A2a adenosine receptor and observed that sub-threshold doses of an inflammatory stimulus caused extensive tissue damage, and more prolonged and higher levels of pro-inflammatory cytokines than in the wild-type mice — where the tissue damage was minimal. In addition, three other different models of inflammation as well as bacterial endotoxin-induced septic shock elicited similar results (Nature 2001, 414:916-920).

"The marked effects of A2a receptor deficiency on functions of immune cells in vivo point to the possible role of A2a receptors in the regulation of different stages of immune responses" concluded the ...