Borrowing Name-Tags: Cholera’s Method of Evading our Defences

The surfaces of animal cells are covered with proteins, sugars, and fats that not only give the cell a spiky appearance, but also have important functions. For example, some of these surface molecules act as a name-tag to identify the cell as “host” and not a threat to the immune system. Other surface molecules act as pores, allowing for the transport of cargo into and out of the cell. These molecular “spikes,” however, are also crucial for infection by acting as docking sites for bacteria and viruses.

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A recent study from Wesleyan University (Connecticut) showed that a toxin from Vibrio cholerae uses membrane sugars to dock to cells, allowing the bacteria to avoid our immune system and make us sick. V. cholerae is an ocean bacterium that can be found worldwide, but prefers warmer water. Upon infection, V. cholerae causes a disease known as cholera, which leads to lots of watery diarrhea (sometimes up to 20 litres a day!) and dehydration. Cholera strikes hardest in the developing world because appropriate treatment (hospitalization and intravenous fluids) can be hard to achieve.

To prevent future cholera outbreaks and devise new treatments, there is a real need to understand how V. cholerae causes disease. This research team not only determined the exact sugars on the outside of the cell necessary for V. cholerae toxin docking, but also the parts of the toxin important for docking to occur. The next steps for these Wesleyan researchers is to devise methods to prevent the bacteria from using these sugars. By doing so, we may eventually be able to prevent disease altogether, or at least treat those infected more efficiently.


Summary written by: Landon Getz


To read the full article, please click the following link:

Structural basis of mammalian glycan targeting by Vibrio cholerae cytolysin and biofilm proteins

Swastik De, Katherine Kaus, Shada Sinclair, Brandon C. Case, Rich Olson

 

 

 

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