Diabetes Mellitus dan Infeksi

DM and Infection: Physiopathology

• Complement system:
• Serum and surface protein -> promote phagocytosis
through macrophages and neutrophils & promote lysis of
the microorganism
• Signals activation of B-lymphocyte and production of
antibody
• DM -> deficiency in the complement system
DM and Infection: Physiopathology
• Polymorphonuclear dysfunction
• Hyperglicemia:
• Decreased mobilization of polymorphonuclear leukocytes, chemotaxis and phagocytic activity
• Inhibits G6PD (antimicrobial function), increases apoptosis of polymorphonuclear leukocytes
• Reduced polymorphonuclear transmigration through the endothelium
• In cells that don’t need insulin for glucose trnaport, increase intracellular glucose level ->
metabolized by NADPH -> NADPH level decreased -> oxidative cell
• Reduced cytokine response
• Mononuclear & monocytes in DM secrete less IL-1 and IL-6 in response to
lipopolysaccharides
• Increased glycation inhibits production of IL-10 by myeloid cells, TNF-a by T cells
• Glycation reduced MHC on myeloid cell surface -> impaired cell immunity
Pathophysiology of Infections Associated with
Diabetic Mellitus