Bacterial Pili exploit integrin machinery to promote immune activation and efficient blood-brain barrier penetration

Anirban Banerjee, Brandon J. Kim, Ellese M. Carmona, Andrew S. Cutting, Michael A. Gurney, Chris Carlos, Ralph Feuer, Nemani V. Prasadarao and Kelly S. Doran ()
Additional contact information
Anirban Banerjee: San Diego State University
Brandon J. Kim: San Diego State University
Ellese M. Carmona: San Diego State University
Andrew S. Cutting: San Diego State University
Michael A. Gurney: San Diego State University
Chris Carlos: San Diego State University
Ralph Feuer: San Diego State University
Nemani V. Prasadarao: Childrens Hospital Los Angeles and University of Southern California Keck School of Medicine
Kelly S. Doran: San Diego State University

Nature Communications, 2011, vol. 2, issue 1, 1-11

Abstract: Abstract Group B Streptococcus (GBS) is the leading cause of meningitis in newborn infants. Bacterial cell surface appendages, known as pili, have been recently described in streptococcal pathogens, including GBS. The pilus tip adhesin, PilA, contributes to GBS adherence to blood-brain barrier (BBB) endothelium; however, the host receptor and the contribution of PilA in central nervous system (CNS) disease pathogenesis are unknown. Here we show that PilA binds collagen, which promotes GBS interaction with the α2β1 integrin resulting in activation of host chemokine expression and neutrophil recruitment during infection. Mice infected with the PilA-deficient mutant exhibit delayed mortality, a decrease in neutrophil infiltration and bacterial CNS dissemination. We find that PilA-mediated virulence is dependent on neutrophil influx as neutrophil depletion results in a decrease in BBB permeability and GBS–BBB penetration. Our results suggest that the bacterial pilus, specifically the PilA adhesin, has a dual role in immune activation and bacterial entry into the CNS.

Date: 2011
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DOI: 10.1038/ncomms1474

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