One of bacteria’s attack tactics has been revealed: they can deploy molecules that bind to and switch off mucous-oozing cells.
A team of researchers in Germany found how some microbes use special proteins that give them a foothold on slippery surfaces.
For much of the body, such as lungs, intestine, throat, nose and genital tract, mucosal linings are the first points of contact for pathogens.
Animals, including humans, shed top layers of those areas quickly, so any microbes that gain a foothold simply slip off.
But some bacteria seem to get around that hurdle.
Christof Hauck from the University of Konstanz and colleagues had already shown that Neisseria gonorrheae, the bacteria behind gonorrhoea, suppressed exfoliation.
Reporting in PLOS Pathogens today, they genetically engineered Escherichia coli bacteria to start pumping out Opa proteins – something they don’t normally do.
And in a dish in the lab, they saw the E. coli act more like N. gonorrheae and stopped mucosal cells from sloughing off.
They repeated the experiment in mice genetically engineered to exude high levels of a protein called CEACAM (carcinoembryonic antigen-related cell adhesion molecules) on their mucosal surfaces.
CEACAM is found in human mucosal cells and is a protein to which the bacterial Opa latches.
Some 24 hours after vaginal infection with Opa-expressing E. coli, the animals’ mucosal surfaces were brimming with bacteria, showing successful colonisation by the bacteria.
Those expressing only the mouse version of CAECAM, though, didn’t have nearly as many E. coli stuck to them. And non-genetically engineered E. coli also failed to colonise mice expressing human CAECAM.
Unpicking bacteria’s tactics, the researchers write, could help shape better prevention and treatment drugs.
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