Proposed mechanism used by S aureus to interact with B1R and B2R. Based on the results of the present study, the following model is suggested. At the infectious site, invading monocytes become activated by staphylococcal toxins and secrete proinflammatory cytokines that induce an up-regulation of the B1R at the infectious focus. Plasma exudation into the infectious site will trigger contact activation and the formation of BK. BK can bind to B2R and trigger its down-regulation or be converted to the B1R agonist, desArg⁹BK, which subsequently leads to an activation and an additional up-regulation of B1R.