The angiotensin II AT1 receptor is not the major pathway for increased bacterial resistance in Neu^ACEmice. (A-B) Superoxide production was measured by cytochrome c reduction in neutrophils isolated from bone marrow following a 5-hour in vitro challenge with MRSA (1 × 10⁶ CFU/mL). As a control, samples were treated with 15 µg/mL SOD to eliminate superoxide. (A) Some mice were pretreated with the AT1 receptor antagonist losartan for 1 week (600 mg/L in drinking water) and during superoxide measurements (100 µM). (B) Other mice were pretreated with the ACE inhibitor ramipril for 1 week (36.3 mg/L in drinking water) and during superoxide measurement (1 µM). In both panels A and B, n = 5/group. (C) MRSA skin infection with losartan treatment. Mice were infected subcutaneously with MRSA (2 × 10⁸ CFU/mouse flank). Some mice were treated with losartan as described in panel A. The drug was continued during the experiment. (i) Skin lesion area, (ii) bacterial burden at day 3. (D) MRSA skin infection with aliskiren treatment. Mice were treated IP with the renin inhibitor aliskiren for 5 days (25 mg/kg per day, 1 dose/day) and then infected with MRSA as in panel C. Aliskiren was continued during the experiment. (i) Skin lesion area, (ii) bacterial burden at day 3. *P ≤ .05, **P ≤ .005, ***P ≤ .0005.