Abstract
Diabetes mellitus predisposes to variety of infectious diseases. The risk for pyogenic infections is increased 2aEuro to 4aEurofold, with Staphylococcus aureus being among the most important pathogens. Apart from comorbidities, dysfunction of the immune system leads to an increased susceptibility to infections. Despite conflicting results, several disturbances of the immune system have been ...
Abstract
Diabetes mellitus predisposes to variety of infectious diseases. The risk for pyogenic infections is increased 2aEuro to 4aEurofold, with Staphylococcus aureus being among the most important pathogens. Apart from comorbidities, dysfunction of the immune system leads to an increased susceptibility to infections. Despite conflicting results, several disturbances of the immune system have been described. Impairments of granulocyte function comprise reduced chemotaxis, phagocytosis, and bacterial killing with reduced oxidative burst. Decreased pathogen-induced granulocyte apoptosis leads to prolonged inflammation and production of inflammatory cytokines. Lower IgG (Ig: immunoglobulin) levels and inhibition of complement activation and opsonization are found on the side of the humoral immune response. Disturbed prostaglandin E2 production leads to a reduced maturation of dendritic cells and a lower Th17 response (Th17: T helper 17 cell). Additionally, evidence suggests that pathogens adapt to increased glucose concentrations with altered gene expression and increased virulence. A multifactorial genesis of the increased susceptibility to infections observed in patients with diabetes mellitus is assumed. Besides predisposing comorbidities mainly disturbances of the innate immune system in combination with the virulence of typical pathogens form the basis of the increased incidence of pyogenic infections.
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