= Discovery stage. (17.55%, 2019 US)
= Translation stage. (42.72%, 2019 US)
= Clinically available. (39.74%, 2019 US)
MSACL 2019 US : Campeau

MSACL 2019 US Abstract

Self-Classified Topic Area(s): Microbiology

Mapping Pathogenesis: A Systems-Level Investigation of GBS Meningitis

Anaamika Campeau (1,2,3), Liwen Deng (4,5), Patrick Schupp (6), Robert Mills (1,2,3), Michael Oldham (6), Kelly Doran, (5), David Gonzalez (1,2,3)
(1) Department of Pharmacology, (2) Skaggs School of Pharmacy and Pharmaceutical Sciences, (3) Center for Microbiome Innovation, University of California, San Diego, La Jolla, CA 92093, (4) Department of Biology, San Diego State University, San Diego, CA, (5) Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, (6) Department of Neurological Surgery, University of California, San Francisco, San Francisco, CA.


Warning: Undefined variable $headshot in /var/www/html/view_abstract/view_abstract_in_program.php on line 704
 Anaamika Campeau (Presenter)
UC San Diego

Presenter Bio: Anaamika Campeau grew up in Moorpark, CA. She attended UC Berkeley for her undergraduate studies, majoring in Molecular and Cell Biology. She holds a Master's Degree in Experimental and Molecular Pathology, and is currently pursuing her PhD in Biomedical Sciences at UC San Diego.

Relevant Financial Disclosures (within past 24 months)
Grant/Research Support UC San Diego
Salary UC San Diego

Abstract

Group B Streptococcus (GBS) remains the primary causative agent in neonatal meningitis, a condition which can result in long-term neurological impairment. We performed quantitative mass spectrometry-based proteomics on tissues from GBS-infected mice. Analysis of the blood proteome during infection revealed comprehensive immune suppression during systemic infection. Infected brain tissue showed unique infection- and invasion-associated protein abundance changes, with invasion-competent bacteria inducing endothelial changes associated with development. Pathogenesis was further studied in vitro, where caveolin-dependent membrane remodeling was necessary for bacterial invasion of brain endothelial cells. These findings underscore the investigative potential of systems biology strategies for understanding pathogenesis.