Published online 3 June 2002. doi:10.1083/jcb1576rr1
© The Rockefeller University Press,
0021-9525/2002/6/906 $5.00
The Journal of Cell Biology, Volume 157, Number 6, June 10, 2002 906-906
Getting sick from Sic
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Bacteria with Sic (black bar) escape killing by phagocytes.
Musser/NAS
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Letting go may be hard to do, but Nancy Hoe, James Musser (National Institutes of Health, Hamilton, MO), and colleagues have found that certain successful Streptococci actually avoid attachment to host cells. This contrasts with the modus operandi of most pathogenic bacteria.
The M1 serotype of the highly heterogeneous Group A Streptococcus (GAS) pathogen is the most common GAS strain found in severe disease outbreaks. M1 GAS are unique in that they produce streptococcal inhibitor of complement (Sic), the loss of which impairs the ability of the pathogen to colonize the upper respiratory tract of mice. "The old dogma was that successful colonization necessarily involves adherence," says Hoe. "That's what led us to look at Sic, to see if it helps the bacteria adhere to host cells."
Unexpectedly, Sic inhibited adhesion to human epithelial cells. Sic was internalized into host cells, where it interacted with ezrin and moesin, proteins that link actin to the plasma membrane during the formation of microvilli. Host cells containing Sic lost their microvilli, structures that may be important for GAS–host cell interaction. Bacteria lacking Sic were also more susceptible to phagocytosis (another actin-dependent process) by leukocytes. Hoe believes Sic is important early in infection, when few bacteria are present and maintaining numbers is crucial. This enhanced ability to persist contributes to the ability of M1 GAS to cause epidemics. 
Reference:
Hoe, P., et al. 2002. Proc. Natl. Acad. Sci. USA. 99:7646–7651.[Abstract/Free Full Text]
Nicole LeBrasseur
lebrasn{at}rockefeller.edu
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