Once thought of as a hero, now also a villain - that’s the way researchers are now looking at a cytokine called interleukin IL-17A and its role during certain infections that lead to Toxic Shock Syndrome (TSS).
TSS is a life-threating inflammatory response brought on by systemic exposure to bacterial superantigens, which are toxins harbored and secreted by certain common bacteria, namely staph and strep bacteria. The inflammatory response triggered by the immune system and its consequences, such as profound immunosuppression, are what make TSS fatal.
Previously, the cytokine IL-17A was only thought to play a protective role in Gram-positive bacterial infections, including those caused by superantigen-producing bacteria, by flushing out the site of the infection. However, researchers at Schulich Medicine & Dentistry have now shown that this is not the only way IL-17A participates in superantigen-mediated illnesses.
“IL-17A is known for its role in facilitation of the recruitment of certain white blood cells to the site of infection,” said Mansour Haeryfar, associate professor, Microbiology and Immunology. While this function of IL-17A promotes the elimination of bacteria and clearing infection in many cases, it could actually play a disease-causing role when seen in the context of exposure to superantigens that cause TSS among other illnesses.
Hearyfar and his team found that this cytokine causes exaggerated inflammation during TSS, which can result in organ failure or even death. By targeting IL-17A specifically, they were able to shut down some of the adverse effects, thus significantly improving morbidity and survival rates in an animal model of TSS. They were also able to repeat their findings using human white blood cells.
“The next step will be to explore the benefit of using IL-17A-targeted therapies, especially in combination with treatments that block the harmful action of other inflammatory mediators,” said Haeryfar. “Our hope is that these treatments can potentially enter clinical trials for TSS and similar inflammatory conditions.”
The study created quite a buzz in the scientific community, recognized as among the top 10 per cent of articles published in The Journal of Immunology, the flagship publication of the American Association of Immunologists, and also highlighted by the Faculty of 1000 – a platform for top researchers to share important and game-changing research with each other.