**12. Phagocytosis**

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.

that an optimal diabetes regulation possibly can improve the host response.

In vitro tests analysing the functions of non-diabetic polymorphonuclear cells (PMNs) are carried out by incubating these cells with plasma derived from patients with DM. These defects are not correlated with the amount of glucose present in plasma [6, 25, 26]. An example is the increased adherence of PMNs of non-diabetic patients to bovine aortic endothelium in the presence of diabetic plasma [27]. This increased adherence probably leads to a decrease in diapedesis and exudate formation of PMNs [27]. The question arises which factor in diabetic serum is responsible for the difference mentioned above. It has been suggested [28] that AGEs play a role. Since the formation of AGEs is increased in poorly regulated patients, it seemed

Another frequently mentioned substance in the pathogenesis of infections in diabetic patients is zinc. Low plasma zinc levels have been reported in DM type 1 and type 2 patients [6]. Nevertheless, in another study, no differences in zinc levels between diabetic and nondiabetic subjects were found [29]. In vitro studies described a disturbed lymphocyte response and depression of chemotaxis in diabetic PMNs when zinc deficiency was present [1, 6, 28]. Other in vitro studies with PBMCs of non-diabetic patients showed an enhanced LPSinduced excretion of pro-inflammatory cytokines after the addition of zinc [30]. Considering the contradictory epidemiological data about zinc deficiency in DM patients, the clinical relevance of the above-mentioned in vitro results in the pathogenesis of infections in diabetic

In conclusion, some innate (cytokines, complement) humoral immune functions are decreased

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

and some remain the same in patients with DM compared to those without DM.

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

**9. Other serum factors**

20 Ultimate Guide to Insulin

patients remains unclear.

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