**10. Cellular innate immunity: PMNs and chemotaxis**

A significantly lower chemotaxis has been found in PMNs of diabetic patients (type 1 and type 2) than in those of controls [25, 31, 32]. However, it could not be demonstrated in the study in which (we studied) the PMN function in women with DM having asymptomatic bacteriuria were compared to non-bacteriuric diabetic women (healthy controls) were studied [33]. All studies used serum from healthy controls. It is possible that the different stimuli (zymosan, complement) of the PMNs and the differences in patient characteristics (duration, regulation and complications of DM, DM type 1 or DM type 2) in the above-mentioned studies may explain these contradictory results. No correlation was found between glucose concentration [25, 32] or haemoglobin A1c (HbA1c, which is a serum marker for the regulation of the DM) level and the chemotactic responses, although one study showed a further reduction in chemotaxis in patients with hyperglycaemia [31]. Interestingly, one of the other studies showed that the chemotactic responses of the PMNs did not alter after the incubation of either glucose or insulin, but returned to normal values after the incubation with glucose and insulin together [32]. Since most PMN functions are energy-dependent processes [34], an adequate energy production is necessary for an optimal PMN function. Glucose needs insulin to enter the PMNs to generate this energy, which may explain the improvement of the chemotactic response after the addition of these two substances.
