Enterococcus faecalisis an opportunistic pathogen that is frequently co-isolated with other microbes in wound infections. WhileE. faecaliscan subvert the host immune response and promote the survival of other microbes via interbacterial synergy, little is known about the impact ofE. faecalis-mediated immune suppression on co-infecting microbes. We hypothesized thatE. faecaliscan attenuate neutrophil-mediated responses in mixed-species infection to promote survival of the co-infecting species. We found that neutrophils controlE. faecalisinfection via phagocytosis, ROS production, and degranulation of azurophilic granules, but it does not trigger neutrophil extracellular trap formation (NETosis). However,E. faecalisattenuatesStaphylococcus aureus-induced NETosis in polymicrobial infection by interfering with citrullination of histone, suggestingE. faecaliscan actively suppress NETosis in neutrophils. ResidualS. aureus-induced NETs that remain during co-infection do not impactE. faecalis, further suggesting thatE. faecalispossess mechanisms to evade or survive NET-associated killing mechanisms.E. faecalis-driven reduction of NETosis corresponds with higherS. aureussurvival, indicating that this immunomodulating effect could be a risk factor in promoting the virulence polymicrobial infection. These findings highlight the complexity of the immune response to polymicrobial infections and suggest that attenuated pathogen-specific immune responses contribute to pathogenesis in the mammalian host.