How pathogenic bacteria hide inside host cells

Written by: Ani
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Washington, Jan 27 (ANI): Scientists have demonstrated how bacteria developed a strategy of hiding within host cells to escape the immune system as well as many antibacterial treatments.

The study carried out in Staphylococcus aureus, the bacterium which is responsible for severe chronic infections worldwide, shows how 'phenotype switching' enables bacteria to adapt to their environmental conditions, lie dormant inside host cells and become a reservoir for relapsing infections.

Staphylococcus aureus is a major human pathogen, which can be carried by up to 70 percent of healthy people, and can lead to conditions such as deep tissue infections, osteomyelitis, and chronic lung infections, which are often hard to treat with antibiotics.

A key characteristic of these infections is that relapses can occur months or years after an apparent cure.

Bettina Loffler and her team from the Institut fur Medizinische Mikrobiologie in Munster, Germany, believe these relapses are due to phenotype switching, a change in the bacterial behaviour.

After infection and invasion of the patient's host cells, the bacteria form small colony variants (SCVs), tiny bacterial subpopulations that can evade the immune system as well as many antibiotics and grow slowly.

The team performed long-term infection studies with Staphylococcus aureus in cell culture systems and also analysed tissue samples from subacute and chronic human infections.

The research revealed that in all infection models, the bacteria were able to persist within the host for several weeks after the infection, leading to the formation of SCV colonies.

This showed that SCVs began to appear following infection, after the immune system response was overcome and that this persistence led to a larger phenotypic diversity of bacteria.

This process enables the bacteria to hide inside host cells without provoking an inflammatory response from the host's immune system. In addition, they might be efficiently protected from antibiotic treatment.

The findings were published by EMBO Molecular Medicine. (ANI)

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