Table 1.
Influence of diabetes/hyperglycemia on innate and adaptive immunity and other factors
| System | Impaired organ/cell | Main effects | Selected references |
|---|---|---|---|
| Innate immunity | |||
| Cellular | Neutrophils, monocytes, and macrophages | Dysfunction in adhesion, transmigration, chemotaxis, phagocytosis, microbial killing, apoptosis, and capability of antigen presentation | (5–8,11) |
| Humoral | Complement | Low or high levels of several complement components | (14) |
| Cytokines | Baseline increased levels of TNF-α, IL-6 | ||
| Impaired cellular (in vitro) cytokine production of TNF-α, IL-1β, IL-8, IL-6, IFN-γ at baseline and under LPS stimulation (increased or decreased) | (8) | ||
| Impaired sequential patterns of cytokine production | (9) | ||
| Impaired local cytokine production | (10) | ||
| Adaptive immunity | |||
| Cellular | T-cells | Impaired response against different antigens | (12,13) |
| Humoral | Immunoglobulins | Quantitative defects: decrease in amount of global and specific antibodies | (14,53) |
| Qualitative defects: glycosylation of antibodies, impaired humoral responses | (13,15) | ||
| Endothelium | Reduction in vasodilatation response; inflammatory endothelial activation: increased levels of adhesion molecules (VCAM-1, ICAM-1, E-Selectin) | ||
| (5,8,22–24, 54,55) | |||
| Coagulation | Induction of a procoagulant state: increased levels of TFP activity, FVIIa, FVIII, thrombin-antithrombin complexes, von Willebrand factor, TFPI activity, and a decrease in PAI-1 activity | (7,23,56) | |
| Miscellaneous | Microbial colonization | Increased rate of colonization by pathogenic bacteria (nasal Staphylococcus aureus, pharyngeal gram negative bacteria, yeast) | |
| Other organ systems | Diabetic gastropathy, urinary bladder dysfunction, reduced bronchial reactivity, and diminished bronchodilation | ||
Dysfunctions presented are obtained from literature based on diabetic patient and diabetic animal models. References regarding effect of hyperglycemia on healthy cells (in vitro) or healthy individuals (in vivo) have not been included.
ICAM, intercellular adhesion molecule; LPS, lipopolysaccharide; PAI, plasminogen activator inhibitor; TFP, tissue factor procoagulant; TFPI, tissue factor procoagulant inhibitor; VCAM, vascular cell adhesion molecule.