Type 1 diabetes is a genetic, auto-immune disorder. You can not “catch” diabetes from anyone. Lol. 😛
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Animation Description: Under normal circumstances, bacterial infection results in the release of chemokines that attract circulating neutrophils to the endothelium. This process is known as chemotaxis.
A variety of molecules are expressed on the endothelial cell surface that allow the neutrophil to be captured, then roll along the endothelium, then adhere.
Following adherence, the neutrophil migrates into the subendothelial tissue to reach the site of infection.
The neutrophil engulfs the bacteria and eliminates them via breakdown within the phagosomes — a process known as phagocytosis.
In states of hyperglycemia, chemotaxis is reduced. Adherence is also adversely affected.
Phagocytosis is also impaired by hyperglycemia.
Hyperglycemia also adversely affects the macrophage system. Under normal circumstances, circulating monocytes are attracted to sites of infection, roll, adhere, and then migrate into the subendothelial space. The monocyte then transforms into a macrophage.
which is then activated by cytokines released by the bacteria. The activated macrophage then engulfs the bacteria.
However, hyperglycemia results in decreased activation of macrophages, thereby arresting the process of macrophage phagocytosis of bacteria.
In addition to affecting neutrophil and macrophage function, hyperglycemia also affects the complement cascade. Under situations of normal glycemia, bacteria can activate the complement cascade.
Activation of the complement cascade results in the formation of transmembrane protein channels known as membrane attack complex (MAC) in bacterial membrane.
Membrane attack complexes make the bacterial membrane porous and the rapid influx of fluid results in the bacterial cell death.
Hyperglycemia inhibits the proper activation of the complement cascade, thereby reducing another pathway of the immune system.
