Furthermore, we show that in vivo modulation of the IL-23/IL-17A axis either by administration of exogenous cytokines (IL-17A or IL-23) or IL-17A depleting antibody, does not only result in immune modulation or altered bacterial clearance, but also directly affect resilience of animals to intranasal LVS infection, evident by clinical endpoints such as morbidity patterns (reflected by body weight) and cumulative survival. This evidence concerns the gene IL23A and infection.