Scientists discover how superbugs hide from their host
- New research reveals how a common hospital superbug causes infections – currently poorly understood by scientists
- Scientists at the University of Sheffield uncovered a complex mechanism that enables bacteria to evade the immune system
- Findings could be used to develop new treatments for Enterococcus faecalis infections, which can be life threatening
New research led by the University of Sheffield has discovered how a hospital superbug evades the immune system to cause infection – paving the way for new treatments.
The study, led by the University of Sheffield’s Department of Molecular Biology and Biotechnology, investigated how Enterococcus faecalis (E. faecalis), bacteria commonly found in the digestive tracts of humans, cause life-threatening infections.
While E. faecalis is harmless in healthy carriers, it is also an opportunistic pathogen that frequently causes hospital-acquired infections such as heart valve infections, urinary tract infections and bacteraemia – the presence of bacteria in the blood. Scientists currently do not fully understand how this happens.
Treatment of E. faecalis infection is difficult as it is highly resistant to several key components of the immune system and resistant to multiple antibiotics.
Now, new research led by Dr Stéphane Mesnage from the University of Sheffield’s Department of Molecular Biology and Biotechnology, has discovered a mechanism used by E. faecalis to hide from the immune system of the host.
The study revealed that the bacteria changes a component of its cell surface in order to evade the immune system, enabling the spread of infection. The findings could pave the way for novel treatments for infections caused by E. faecalis.
Dr Stéphane Mesnage, Senior Lecturer in Molecular Biology and Biotechnology, said: “E. faecalis is an opportunistic pathogen. It is naturally resistant to a wide range of antibiotics including synthetic penicillin derivatives and is acquiring resistance to the last resort antibiotic vancomycin. Following an antibiotic treatment, E faecalis can out-compete other microorganisms to cause an infection.
“Our study shows that this organism modifies its polysaccharide surface, which is essential for causing an infection. Bacteria whose polysaccharides are unmodified are quickly recognised and engulfed by the cells of our immune system, whereas by modifying the polysaccharide, E. faecalis can evade the host immune cells and spread infection.”
Dr Mesnage added: “Hospital-acquired infections caused by bacteria resistant to last resort antibiotics are on the rise. Our work suggests that targeting the mechanism that modifies the surface polysaccharides could be a novel strategy for developing new treatments to fight E. faecalis infections.”
The research, Decoration of the enterococcal polysaccharide antigen EPA is essential for virulence, cell surface charge and interaction with effectors of the innate immune system, is published in the journal PLoS Pathogens.
The Department of Molecular Biology and Biotechnology at the University of Sheffield is focussed on studying DNA, RNA (Ribonucleic Acid) and proteins, and how they affect biological function such as host-pathogen interactions. Researchers work on topics from genomics and nucleic acids to plants and photosynthesis, with the aim of addressing the major global challenges of food security, antimicrobial resistance and an aging population. Many of its scientists are following in the footsteps of Sir Hans Krebs, the department’s first Professor of Biochemistry, who was awarded the Nobel Prize in Physiology or Medicine in 1953.
The University of Sheffield
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