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Skin Bacteria a Cause of Diabetes?

Toxin produced by Staphylococcus aureus (S. aureus), a common skin bacteria, caused glucose intolerance in rabbit cells…

Bacteria and viruses have an obvious role in causing infectious diseases, but microbes have also been identified as the surprising cause of other illnesses, including cervical cancer (Human papilloma virus) and stomach ulcers (H. pylori bacteria).

A new study by University of Iowa microbiologists now suggests that bacteria may even be a cause of one of the most prevalent diseases of our time: Type 2 diabetes.

The research team led by Patrick Schlievert, professor and department executive officer of microbiology at the UI Carver College of Medicine, found that prolonged exposure to a toxin produced by Staphylococcus aureus (staph) bacteria causes rabbits to develop the hallmark symptoms of Type 2 diabetes, including insulin resistance, glucose intolerance, and systemic inflammation.

“We basically reproduced Type 2 diabetes in rabbits simply through chronic exposure to the staph superantigen,” Schlievert says.

The UI findings suggest that therapies aimed at eliminating staph bacteria or neutralizing the superantigens might have potential for preventing or treating Type 2 diabetes.

Obesity is a known risk factor for developing Type 2 diabetes, but obesity also alters a person’s microbiome — the ecosystem of bacteria that colonize our bodies and affect our health.

“What we are finding is that as people gain weight, they are increasingly likely to be colonized by staph bacteria — to have large numbers of these bacteria living on the surface of their skin,” Schlievert says. “People who are colonized by staph bacteria are being chronically exposed to the superantigens the bacteria are producing.”

Schlievert’s research has previously shown that superantigens — toxins produced by all strains of staph bacteria — disrupt the immune system and are responsible for the deadly effects of various staph infections, such as toxic shock syndrome, sepsis, and endocarditis.

The team’s latest study shows that superantigens interact with fat cells and the immune system to cause chronic systemic inflammation, and this inflammation leads to insulin resistance and other symptoms characteristic of Type 2 diabetes. In examining the levels of staph colonization on the skin of four patients with diabetes, Schlievert’s team estimates that exposure to the bacterial superantigens for people who are heavily colonized by staph is proportional to the doses of superantigen that caused the rabbits to develop diabetes symptoms in the team’s experiments.

“I think we have a way to intercede here and alter the course of diabetes,” Schlievert says. “We are working on a vaccine against the superantigens, and we believe that this type of vaccine could prevent the development of Type 2 diabetes.”

The team also is investigating the use of a topical gel containing glycerol monolaurate, which kills staph bacteria on contact, as an approach to eliminate staph bacteria from human skin. They plan to test whether this approach will improve blood sugar levels in patients with prediabetes.

The researchers injected New Zealand White rabbits with either a sub-lethal dose of S.aureus’s toxin: TSST-1 (toxic shock syndrome toxin-1) or phosphate-buffered saline. Weekly, the rabbits also received subcutaneous injections of glucose and their ability to metabolize glucose was measured using a conventional glucometer.

The group of rabbits that were treated with TSST-1 exhibited a persistent worsening of their ability to metabolize glucose as compared to the control group (buffered-saline injected group) starting at week 2 and continuing to deteriorate until the end of the experiment. At the sixth week, the pancreas and the spleen of the TSST-1-treated rabbits were also examined; evidences suggested normal beta-cell function but increased insulin transcription, which indicated insulin resistance in the animals. Furthermore, gross anatomy of the spleens appeared to be enlarged and there were also increased levels of tumor necrosis factor alpha (TNF-alpha) in TSST-1-treated rabbits indicating chronic inflammation was presented.

According the study, “prolonged exposure to TSST-1 induced chronic inflammation, elevated the endotoxin levels in the circulation, and impaired glucose tolerance, all of which are conditions seen in type 2 diabetes patients.”

Practice Pearls:

  • There is an increase in S. aureus colonization in obese individuals.
  • Toxin produced by S. aureus induces chronic systemic inflammation and insulin resistance in rabbits treated with TSST-1.
  • Increased colonization of S. aureus in obese population may contribute to the development of the type 2 diabetes.

Bao G. Vu. Chronic Superantigen Exposure Induces Systemic Inflammation, Elevated Bloodstream Endotoxin, and Abnormal Glucose Tolerance in Rabbits: Possible Role in Diabetes. mBio doi: 10.1128/mBio.02554-14. 24 February 2015 mBio vol. 6 no. 2 e02554-14.