Klebsiella pneumoniae is an opportunistic pathogen that causes a range of infections in locations including the urinary tract, lungs, and liver. The number of life-threatening infections caused by multi-drug resistant strains is increasing rapidly. Additionally, many K. pneumoniae strains possess the ability to evade the hosts immune system. These immune evasion mechanisms aid in damage of host tissue, increase levels of inflammation, and aid in the dissemination of bacterial cells which all can lead to major health complications. A mechanism of importance is the release of outer membrane vesicles by K. pneumoniae. Outer membrane vesicles are produced by all Gram-negative bacteria, and act as a delivery system for the movement of biologically active components across the body and into host cells. They are thought to aid in the evasion of the immune response, by acting as a decoy to whole cells, conferring protection against antimicrobial peptides and the complement cascade. Whether K. pneumoniae derived outer membrane vesicles control and modulate the immune response by trafficking virulence factors into macrophages remains unknown. To observe these interactions and determine how K. pneumoniae outer membrane vesicles can manipulate macrophages, outer membrane vesicles were isolated, and then used to treat bone marrow-derived macrophages in order to monitor trafficking of virulence factors, cell death, and inflammatory responses. Results from these experiments established that K. pneumoniae outer membrane vesicles are trafficked to the inside of macrophages, however limited cell death occurs, unless vesicles are pre-treated to expose its contents such as heath treatment. When pre-treated higher levels of cell death occur across multiple strains of K. pneumoniae. However, through the use of inhibitors such as QVD and MCC950 it was determined that different strains of K. pneumoniae induce different types of programmed cell death, similar to what is seen in mouse infection models with different clinical strains. Characterisation of this host-pathogen interaction between macrophages and K. pneumoniae outer membrane vesicles provides further insight into how K. pneumoniae infections are able to persist and how activation of the innate immune response is evaded in order