While further work is in need to elucidate exact functions of multiple mediators of the adenosine signaling events, the studies outlined in this review support the notion that extracellular adenosine generated by CD39 and CD73 and its subsequent activation of certain subtypes of adenosine receptors may lead to a serious modulation of inflammatory responses, which can favor bacterial life and broaden the impact of infection (Table 1). This evidence concerns the gene ENTPD1 and infection.