Polyunsaturated fatty acids (PUFA) are highly abundant at the host-pathogen interface. Many immune cells, including macrophages, dendritic cells, and neutrophils, release millimolar concentrations of arachidonic acid (AA) upon activation by pathogen-associated molecular patterns. AA is one of the most abundant fatty acids at the host-pathogen interface. Most free AA is converted to bioactive lipid signaling molecules like prostaglandins through the enzymatic activity of the cyclooxygenase enzymes or to leukotrienes and hydroxyeicosatetraenoic acids (HETEs) through the enzymatic activity of leukotrienes. AA is also susceptible to non-enzymatic, autoxidation forming isoprostanes and HETEs, which are structurally similar to enzymatically derived prostaglandins and HETEs, respectively. Additionally, autoxidation of AA produces various lipid electrophiles, including aldehydes, γ-ketoaldehydes, and α,β-unsaturated carbonyls. These lipid electrophiles react with nucleophilic groups on cellular macromolecules, potentially altering the biological function of the target molecules. We discovered that AA is bactericidal against S. aureus through a lipid peroxidation mechanism and that preventing lipid electrophile formation abrogates the toxicity of AA against S. aureus. Future studies in the lab will further define the role of bactericidal lipid electrophiles in controlling S. aureus infections.