Since B. burgdorferi is protected from the cytotoxic effects of the neutrophil respiratory burst in vivo and in vitro [66–71], it is most likely that inhibition of other neutrophil activities is responsible for reduced B. burgdorferi killing in hyperglycemia, such as reductions in NET formation, C3-dependent phagocytosis and production and activation of BPI and elastase [66,72–76]. This evidence concerns the gene BPI and Hyperglycemia.