Inflammation and Bacteria as a Risk for Developing Diabetes

University of Iowa researchers have published a study using immortalized fat cells to show how bacterial toxins can promote diabetes. The process involves bacterial toxins, such as the LPS-layer of E. coli cell walls, interacting with fat to produce inflammation. The bacterial toxins cause cellular release of cytokines that promote this inflammation. This is very harmful to the body due to its persistence and leads to insulin resistance. The researchers focused on Staphylococcus aureus since it is the most prevalent colonizing bacteria in diabetes and diabetic foot infections. The superantigens that are produced by S. aureus promote cytokine release and inflammation that is essentially amplified by fat cells, furthering diabetes development.

The superantigens aren’t detoxified from the cells by the same manner as the LPS detox pathway, however, that is seen in E. coli. This leads to chronic inflammation that results in marked insulin resistance in the fat cells. Moreover, the combination of superantigens and LPS magnified the inflammatory response. Thus, the results show that this chronic inflammation is tied to both impaired glucose tolerance and diabetes development. Also, diabetic wound healing could be adversely affected, leading to amputation.

Practice Pearls:

• Bacterial superantigens, such as those produced by S. aureus, were shown to produce chronic inflammation in immortalized fat cells in vitro.
• Obesity causes greater Staph colonization commonly found in diabetic foot ulcers.
• Chronic inflammation leads to increased insulin resistance, leading to diabetes development and poor wound healing.

PLOS ONE, November 2013