Stress Hyperglycemia, Insulin Treatment, and Innate Immune Cells
Table 1
Effects of hyperglycemia and insulin on innate immune cells.
Hyperglycemia
Insulin
Monocyte
(1) Generally enhances cytokine production [7–10, 13–15] (2) Regulates adhesion, migration, and transmigration [13, 14, 17]
(1) Enhances pathogen clearance [34, 35] (2) Promotes IL-8/CXCL8 secretion [38] (3) Increases superoxide production [40] (4) Promotes TNF-α and IL-6 secretion in the presence of palmitate [37] (5) Regulates monocyte metabolism by increasing the phagocytosis of oxidized low-density lipoprotein [36, 37]
Macrophage
(1) Promotes proliferation [18, 19] (2) Enhances cytokine production and phagocytosis in response to LPS in vitro [16, 20] (3) Impairs proinflammatory cytokine secretion, such as TNF-α and IL-6 ex vivo [21]
(1) Inhibits TNF-α, IL-1, and IL-8 secretion [42, 44] (2) Reduces macrophage accumulation in tissue [43] (3) Promotes human macrophage foam cell formation [47, 48]
Neutrophil
(1) Inhibits neutrophil function such as degranulation [25–27] (2) Downregulates production of myeloperoxidase (MPO) [25]
(1) Increases the total number of PMN and their surface expression of CD11b, CD115, CD62L, and CD89 [50] (2) Increases PMN function including chemotaxis, phagocytosis, and bactericidal capacities [50, 51]
