About This Project

Ask the Scientists

What is the context of this research?

Research into the microbiome has uncovered that the bacteria that colonize our bodies can have profound effects on various processes vital to our well being. Disrupting the native microbial ecology of our bodies can lead to disease. Studies indicate up to 50% of the human population is colonized with Staphylococcus aureus at any given time. Human skin and mucosal surfaces are the most common areas of colonization. This organism produces a unique class of toxins known as superantigens that interact with the immune system to cause localized and systemic inflammation. Cardiovascular disease and type 2 diabetes are characterized by systemic inflammation. The role of the S. aureus superantigens in the development of type 2 diabetes and cardiovascular disease has not been fully explored.

What is the significance of this project?

Bacterial infections that lead to disease have been thought of as an acute state of disrupted homeostasis that can be resolved by treatment with antibiotics. Research involving the microbiome indicates that some chronic diseases may be the result of byproducts of long term infection. S. aureus can colonize individuals without leading to illness and those suffering from type 2 diabetes or develop cardiovascular disease are often very heavily colonized. The superantigens produced by S. aureus are known to act systemically inducing a state of acute inflammation but their role in chronic inflammation observed in type 2 diabetes and cardiovascular disease is unknown. Information about the role of these proteins in chronic disease could lead to treatments such as vaccines and targeted therapies.

What are the goals of the project?

The primary goal of this project is to determine if superantigens have the ability to cause cardiovascular disease and type 2 diabetes through induction of systemic inflammation. Inflammation induced by these proteins will be measured by:
1. Tissue culture using aortic endothelial cells to identify if they have direct interactions that cause cell damage or disruption.
2. Measuring the uptake and clearance of glucose from adipocytes isolated from toxin treated model systems.
3. Characterizing systemic inflammation induced by superantigens using established immunological markers.
4. Identifying compounds that can be used to decrease of eliminate inflammation caused by superantigen exposure. These findings will provide a basis for further study of the role of superantigens in chronic disease.