Bacterial meningitis is the most common nervous system infection and a major cause of childhood death. In a new study appearing in the September 1 print issue of The Journal of Clinical Investigation, Kelly Doran and colleagues from UCSD investigate the mechanisms responsible for the penetration of the human blood-brain barrier (BBB) by Group B Streptococcus (GBS), the bacteria that causes meningitis in newborn infants.

The authors find a novel GBS gene, called iagA, which helps the bacteria invade the normally shield-like brain endothelial cells of the BBB. An iagA mutant showed decreased invasion through these cells and reduced the development of meningitis and lethality in vivo. Deletion of iagA did not affect other key steps in the pathogenesis of GBS meningitis, including bacterial survival. Thus iagA specifically promotes endothelial cell uptake of the pathogen. The iagA gene product seems to synthesize a glycolipid anchor that facilitates the bacteria's interaction with the host cell.

In an accompanying commentary, Miriam Baron and Dennis Kaspar write, "this work contributes to our understanding of the molecular pathogenesis of invasive GBS infection. Specifically, the identification of the iagA gene product as a major contributor to GBS invasion and virulence is an exciting development."

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Contact: Stacie Bloom
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
1-Sep-2005

Page: 1
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