Significance Mechanisms for why influenza A virus (IAV) infections sensitize for pneumococcal infections are not clear. Here, we show that IAV-induced capillary leakage results in influx of nutrients and antioxidants to the lungs, thereby promoting pneumococcal growth in the lower respiratory tract. The evoked inflammation leads to redox imbalances that require bacterial adaptation to the oxidized environment, including induction of the pneumococcal chaperone/protease HtrA that protects the bacteria from clearance by the immune system. The results give us insight into the delicate interplay between the bacteria and the host environment during coinfections that needs to be explored in order to find novel therapeutic approaches.