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13 May 2022

Bacteria that cause dysentery also actively block body's ability to fight the infection

Scientists reveal that Shigella tricks the immune system, hindering the body’s ability to mount an effective immune response against infection


Bacterial infections, such as dysentery caused by Shigella, are responsible for millions of deaths each year, but whether these bacteria are also able to interfere with the body’s ability to fight the infection was previously unknown.

Researchers from the Schools of Immunology & Microbial Sciences and Basic & Medical Biosciences at King’s have shed light on the molecular process by which bacteria prevent cells from recognising impending infection.

During infections, the cells which make up our body’s first line of defence release 'interferons’. These warn neighbouring cells and prepare them to fight off an incoming infection. Many viruses – including SARS-CoV2 – have evolved proteins which inhibit normal interferon functions to infect us and spread within the population.

The study, published today in Cell, found that Shigella inject proteins into host cells termed ‘OspCs’ that block the host interferon response. This allows Shigella to successfully infect the host.

Interestingly, OspCs blocked interferon signaling by preventing cells from adapting to changing concentrations of calcium – a molecular signal that usually warns a cell of infection and damage.

This is a newly identified strategy to trick our immune system and prevent us from mounting an effective immune response to infection by decoding host calcium signals.

This study was another perfect example of how studying pathogens can not only lead to a better understanding of infectious processes, but can also reveal the complexity of host responses to infection”

Dr Charlotte Odendall

The researchers assert that these observations may open the door to the development of new treatments for bacterial infections.

Read the full paper: A Family of Conserved Bacterial Virulence Factors Dampens Interferon Responses by Blocking Calcium Signaling

In this story

Charlotte  Odendall

Sir Henry Dale Fellow

Joseph Wanford

Research Fellow

Research Associate

Julien Bergeron

Senior Lecturer