Golden Staph could be ‘fooling’ the body in the development of autoimmune disease

A study led by Professor Richard Kitching from the Centre for Inflammatory Diseases has found that the body may be ‘’fooled’’ by a plasmid-derived protein from some types of Staph aureus (golden Staph), resulting in the development of severe autoimmune disease.


Autoimmune diseases affect over 7% of people and occur when the immune system produces antibodies and immune cells that attack the body's own tissues - resulting in inflammation and damage. While a lot is known about what happens in autoimmune disease, much less is known about how immune tolerance is broken and how autoimmunity occurs.

The study discovered that a protein within plasmids found in Staph aureus can cause loss of tolerance and induce autoimmune vasculitis through a process known as molecular minimcry. During molecular mimicry a bacterial protein “confuses” the immune system by cross reacting with a “self” protein (or autoantigen), leading to the development of autoimmunity.

While plasmids are best known for their roles in antibiotic resistance, this study now links them to autoimmune disease, specifically ANCA-associated vasculitis (AAV), a severe autoimmune disease caused by autoimmunity to myeloperoxidase (MPO).

“People with vasculitis suffer considerable problems - both from the disease itself and from the side effects of non-targeted treatments. This research may help prevent disease relapses and eventually lead to more specific and personalised treatments for disease.” Professor Kitching said.

“It provides further evidence that targeting a specific part of MPO - to dampen rather than activate immune responses – is a viable and sensible strategy in developing more targeted treatments. These new treatments could affect only the “bad parts” of the immune system that cause autoimmunity, while leaving alone the parts of the immune system that protect us from infection and cancer,”

In addition to the involvement of Professor Kitching’s and Professor Stephen Holdsworth’s research team, the study was conducted across several disciplines in collaboration with Professor Anton Peleg, Head of Infectious Diseases at The Alfred Hospital and Monash University, Professor Jamie Rossjohn and Dr Hugh Reid from the Monash Biomedicine Discovery Institute, and Professor Lars Fugger from Oxford University.

The study was funded by the NHMRC, including via the EU RELENT (RELapses prevENTion in chronic autoimmune disease) Consortium, where Professor Kitching works with one of the other RELENT Principle Investigators Professor Peter Heeringa of Groningen, The Netherlands.

The findings have been published in Nature Communications