Golden Staph could be ‘fooling’ the body in the development of autoimmune disease
A cross-disciplinary Monash study, led by Professor Richard Kitching from the Centre for Inflammatory Diseases and closely involving Professor Anton Peleg and his post-doctoral fellow Jhih-Hang Jiang from Monash Biomedicine Discovery Institute (BDI), 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 more than seven per cent 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, published in Nature Commmunications, 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 mimicry. 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).
Professor Anton Peleg, a researcher from the Monash BDI and Department of Infectious Diseases, Central Clinical School, was one of the senior authors on this paper. His lab contributed the staphylococcal expertise and all the bacterial genetics and plasmid characterisation work to the study. The team also performed the bioinformatics to assess the prevalence of the peptide of interest in all publicly available S. aureus genomes. Professor Jamie Rossjohn and his team from Monash BDI were also involved in this important study.
“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.
“This work adds to the repertoire of bacterial plasmids, which are usually responsible for transmission of antimicrobial resistance and virulence genes. It now includes autoimmunity,” Professor Peleg said.
“This study was a fantastic demonstration of cross-disciplinary research at Monash,” he said.
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.
Read the full paper in Nature Communications titled A plasmid-encoded peptide from Staphylococcus aureus induces anti-myeloperoxidase nephritogenic autoimmunity.
This article is based on an original article published by the School of Clinical Sciences.
About the Monash Biomedicine Discovery Institute
Committed to making the discoveries that will relieve the future burden of disease, the newly established Monash Biomedicine Discovery Institute at Monash University brings together more than 120 internationally-renowned research teams. Our researchers are supported by world-class technology and infrastructure, and partner with industry, clinicians and researchers internationally to enhance lives through discovery.