**9. Other serum factors**

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

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 patients remains unclear.

In conclusion, some innate (cytokines, complement) humoral immune functions are decreased and some remain the same in patients with DM compared to those without DM.
