Diabetic wound infections are often associated with the presence of bacterial pathogens coupled to an impaired immune response leading to hyper-inflammation. However, the mechanisms by which bacteria trigger inflammation and persist in the diabetic wound remain elusive. Group B Streptococcus (GBS) is one of the most commonly isolated bacteria from diabetic wound infections, but no previous work has been done on GBS in this clinically relevant environment. Here, we develop a murine model of GBS diabetic wound infection to determine how GBS establishes infection and persists in the diabetic wound. We demonstrate that GBS infection of diabetic wounds triggers an inflammatory response, leading to increased levels of inflammatory cytokines and chemokines such as IL-1b and KC (CXCL1) as well as neutrophil markers myeloperoxidase, calprotectin and elastase. GBS strongly upregulates the surface plasminogen-binding protein PbsP in diabetic wound infection, and a ∆pbsP mutant has decreased adherence to immortalized keratinocytes. Finally, we demonstrate that and that PbsP contributes to GBS burden diabetic wound infection and is necessary for increased inflammation in the wound environment. These data are the first to examine GBS in this clinically relevant model, and to link GBS to chronic inflammation in diabetic wound infection.