Distinct defense strategies against interbacterial antagonism underpin Acinetobacter persistence in polymicrobial environments

Despite intense interbacterial antagonism mediated by mechanisms such as the type VI secretion system (T6SS), pathogenic Acinetobacter frequently persist within highly competitive polymicrobial infections. How these pathogens navigate such hostile environments to achieve co-existence remains poorly understood. Here, we show that pathogenic Acinetobacter employ distinct, multifaceted strategies to resist elimination by both distantly related competitors and closely related kin. T6SS-active strains outcompete heterologous bacteria by deploying a large and diverse repertoire of antibacterial effectors. In contrast, some naturally T6SS-deficient strains resist exogenous T6SS attacks by elaborating a unique, high-density polysaccharide capsule (KL34) that functions as an effective physical shield. Most intriguingly, we uncover a mechanism that prevents lethal competition among kins. A conjugative multidrug-resistant plasmid encoding T6SS repressors is transferred into aggressive strains upon T6SS-mediated attack, leading to suppression of their antibacterial activity. We also found that conjugation is induced by T6SS attack, which effectively suppresses attacking kin and promotes co-infection in vivo . Together, these findings reveal a dynamic and multilayer defense program that enables Acinetobacter to withstand interbacterial warfare while facilitating co-existence. Our study establishes a paradigm in which damage-triggered plasmid transfer enforces targeted suppression, reshaping microbial interactions in polymicrobial communities.