**8. Hyperglycaemia/glucosuria**

Following the 1985 WHO criteria, DM is defined as a fasting glucose concentration of at least 7.8 mmol l −1 or a 2-h glucose concentration of 11.1 mmol l −1 or higher [22]. As a result of this, patients with DM (also with medication) very often have hyperglycaemia. This hyperglycaemic environment can enhance the virulence of certain microorganisms. An example is *Candida albicans*, which expresses a surface protein that has great homology with the receptor for complement factor 3b (CR3). Normally, opsonisation of microorganisms takes place by attachment of complement factor 3b (C3b). Receptors on phagocytising cells recognise this bound C3b and attach, thereby initiating ingestion and killing. In a hyperglycaemic environment, the expression of the receptor-like protein of *C. albicans* is increased, which results in competitive binding and inhibition of the complement-mediated phagocytosis [23]. Another example is the presence of glucosuria, as found in poorly regulated patients. We showed [24] that glucosuria enhances bacterial growth of different *Escherichia coli* strains, which probably plays a role in the increased incidence of urinary tract infections in diabetic patients.

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.

Insulin – Overview, Infections and Benefits of Immunization and Insurance

http://dx.doi.org/10.5772/intechopen.81346

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Conflicting data have been reported about the in vitro adherence of diabetic PMNs without stimulation [25, 27, 31, 34, 35]. In contrast, no differences have been found between diabetic and control PMNs after stimulation [27, 31]. No correlation was found between plasma glucose or HbA1c and adherence [25, 27, 31]. However, in a small number of DM type 1 and DM type 2 patients with untreated hyperglycaemia, the decreased adherence of PMNs to nylon fibre columns increased after the hyperglycaemia was corrected [34, 35]. Of course, adherence to nylon fibre columns is not the same as to endothelial cells as a first step in the inflammation reaction. However, again a better regulation of the DM seemed to increase the host response.

PMNs of diabetic patients have shown the same [25, 33] and a lower [31, 36] phagocytotic capacity compared to PMNs of controls. The mean HbA1c concentration was lower (better regulation) in patients without impaired phagocytosis [33] than in those with impaired phagocytosis [31, 36]. One study [36] showed an inverse relationship between the HbA1c levels and the phagocytotic rate. Another study [37] showed that the decreased phagocytosis improved, but did not become normal after 36 h of normoglycaemia. Therefore, it seems that impairment of phagocytosis is found in PMNs isolated from poorly regulated patients and

Chemiluminescence (CL) corresponds to the emission of light directly or indirectly produced in the course of a chemical reaction. This phenomenon is often used to evaluate the oxidative potential of PMNs, a process during which free radicals are synthesised early in the phagocytotic

that better regulation of the DM leads to an improved phagocytotic function.

**11. In vitro adherence of diabetic PMNs**

**12. Phagocytosis**

**13. Oxidative burst**
