Further, an acute glucose challenge of healthy human subjects was shown to induce reactive oxygen species generation in neutrophils, and neutrophils Nilotinib isolated from patients with type 2 diabetes were found to produce increased amounts of reactive oxygen species compared to neutrophils from healthy controls. These data cannot explain the decreased ability to clear bacterial infections shown clinically as well as in the present study. Instead, impaired bacterial clearance might be due to impaired ability to ingest, kill and remove bacteria and debris accumulated during infection. Indeed, impaired leukocyte phagocytosis has been observed in patients suffering from diabetes. This defect was seen already at moderately increased hyperglycemia indicating that it appears in patients suffering from both uncontrolled type 1 and type 2 diabetes. In the present study, we developed a phagocytic assay where leukocytes were recruited to the peritoneal cavity by injection of LPS-coated fluorescent beads, and we could detect, by using flow cytometry, a 50% decrease of leukocyte phagocytosis in alloxan-treated diabetic mice. However, these experimental results need to be confirmed in studies of leukocyte phagocytic abilities in diabetic patients suffering from recurrent bacterial infections. In conclusion, the results presented here suggest that the reduced ability to clear bacterial infections during diabetes is not due to impaired leukocyte recruitment as prolonged hyperglycemia caused increased number of emigrated leukocytes in tissue during basal conditions as well as during acute inflammation. Despite the increased numbers of recruited leukocytes to inflammation in the diabetic mice, the bacterial infection remained for longer periods due to a defect leukocyte phagocytosis. It is a member of the Burkholderia cepacia complex. The Bcc represents at least 17 phylogenetically closely related yet distinct species of bacteria that are commonly found in the environment and can serve as agents for both plant and human infection. Although most Bcc species have been isolated from CF lungs, the two most common are B. multivorans and B. cenocepacia. Infections with certain strains of B. cenocepacia are associated with a variable and unpredictable clinical course ranging from asymptomatic carriage to a rapid decline in clinical condition leading to fatal necrotizing pneumonia and septicemia, also known as epacia syndrome? In our earlier studies, we showed that ET12 strains that cause epacia syndrome?bind to human respiratory mucins via a pilinassociated 22 kDa adhesin protein. This protein is distributed along the shaft of the large, peritrichous appendages known as cable pili. We also showed that the 22 kDa adhesin mediates the adherence of cable-piliated B. cenocepacia to cytokeratin 13, the expression of which is enriched in airway epithelial cells differentiated into the squamous phenotype.