Pathogenic bacteria, like viruses, are accomplished molecular mimics, deploying surface molecules that interact with host-borne proteins in much the same way that endogenous host molecules do. Cywes and coworkers provide another clear example of this kind of adaptation in the ability of encapsulated strains of Streptococcus to bind epithelial cells of the pharynx and cause sore throats.

Although no single component of the bacterium is required for binding to epithelial cells in culture, strains that lack the capsule fail to interact with the host cell receptor CD44 and are avirulent when presented in vivo.

The bacterial capsule contains hyaluronic acid, the identical polysaccharide that is found in normal extracellular matrix and that interacts with CD44 on mammalian cells. Cywes et al. now show that epithelial cells of the pharynx express CD44 and that, when CD44 levels are suppressed using an antisense RNA, streptococci lose their capacity to colonize the throat.

This interaction can also be blocked in vivo by treating mice with exogenous hyaluronic acid or with antibodies to CD44, suggesting therapies that might treat a common source of misery and possibly other, life-threatening forms of streptococcal infection.

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Contact: John Ashkenas
scied@the-jci.org
206-221-5690
Journal of Clinical Investigation
10-Oct-2000