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Riling up the immune system: P. aeruginosa polysaccharide facilitates inflammation

Being wrong isn’t always a bad thing. Take Christopher Columbus: he set out on his voyage expecting to find a shortcut to India, but landed an extended vacation in the Bahamas instead. The authors of an Observation piece just released in mBio were wrong about their assumptions, too, and although they didn’t wind up on a tropical beach, they did earn some important insights into a leading cause of death among cystic fibrosis patients.

Pseudomonas aeruginosa is an opportunistic pathogen that often strikes the lungs, urinary tract, and kidneys of vulnerable individuals. People with cystic fibrosis, in particular, suffer from P. aeruginosa, which, along with other species, can form a thick biofilm on the lining of the lungs that is impossible for the patient to clear.

To cause an airway infection, P. aeruginosa must first deal with the mucus layer and the underlying epithelial cells. The biofilm polysaccharide Psl has been implicated in attachment to these surfaces, and Byrd et al. confirmed that it is required for adherence. The authors also hypothesized that, like many other biofilm polysaccharides, Psl would protect against immune recognition, an ability that could give the pathogen more time to establish itself before the immune system cottons on and gets to work eliminating it. But they found that, together with the protein flagellin, Psl actually facilitates the signaling that leads to inflammation.

Click on the link above to read the rest of the article on our blog, mBiosphere.
 
 

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