subverts the antioxidant defenses of its amoeba host .

, the causative agent of Legionnaires' disease, interacts in the environment with free-living amoebae that serve as replicative niches for the bacteria. Among these amoebae, is a natural host in water networks and a model commonly used to study the interaction between and its host. However, certain crucial aspects of this interaction remain unclear. One such aspect is the role of oxidative stress, with studies focusing on reactive oxygen species (ROS) production by the host and putting less emphasis on the involvement of the host's antioxidant defenses during the infectious process. In this study, we propose to examine the consequences of infection with wild-type or with an isogenic Δ mutant strain, which is unable to replicate intracellularly, on . For this purpose, we looked at the host ROS levels, host antioxidant defense transcripts, and metabolites linked to the amoeba's antioxidant defenses. It is known that WT can block the activation of NADPH oxidase as soon as it enters the macrophage and suppress ROS production compared to Δ mutant strain. In addition, it has been shown in macrophages that WT decreases ROS at 24 h p.i.; here we confirm this result in amoebae and suggest that this decrease could be partly explained by differentially regulated host antioxidant defense transcripts at 6 h p.i.. We also explored the metabolome of infected or not with . Among the 617 metabolites identified, four with reduced abundances during infection may be involved in antioxidant responses. This study suggests that could hijack the host's antioxidant defenses during its replication to maintain a reduced level of ROS.