Iron is essential to bacterial life, but access is restricted during infection, and so bacteria must scavenge iron from the host environment. A primary strategy involves the biosynthesis and utilisation of native siderophores, as well as the uptake of siderophores produced by other microorganisms (xenosiderophores). Cystic Fibrosis (CF) infections are polymicrobial in nature, and S. aureus and B. cenocepacia are prominent bacterial pathogens in the CF lung. B. cenocepacia produces two siderophores, ornibactin and pyochelin. S. aureus also produces two siderophores, staphyloferrin A and B. Ornibactin is a hydroxamate-type siderophore, and S. aureus is known to take up other hydroxamate xenosiderophores via its Fhu system, which consists of two receptors FhuD1 and FhuD2, transmembrane proteins FhuB and FhuG, and an ATPase FhuC.  Using S. aureus mutants unable to synthesize staphyloferrins, we demonstrate that S. aureus utilizes ornibactin as a xenosiderophore in iron limited medium and Synthetic Cystic Fibrosis Medium, which mimics the environment encountered during co-infection in CF lungs. To investigate the mechanism of ornibactin uptake in S. aureus, we utilized mutants and complemented strains targeting the Fhu system. Mutants lacking either FhuG or the xenosiderophore receptor FhuD2 were unable to acquire iron via ornibactin, whereas deletion of the FhuD1 receptor did not impair ornibactin utilization. Our findings demonstrate that S. aureus can utilise the B. cenocepacia-derived siderophore ornibactin to acquire iron under conditions mimicking CF lung infections. Ornibactin utilisation is mediated through the Fhu uptake system, specifically through the FhuD2 xenosiderophore receptor, highlighting a competitive interspecies interaction during co-infection.