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Julie L. Badger

Assistant Professor
Pathology, Pediatrics
School of Medicine, Childrens Hospital Los Angeles

Send E-mail to:   jbadger@chla.usc.eduWebpage: http://www.childrenshospitalla.org/body.cfm?id=8
Telephone: 323-669-4625Fax: 323-660-9321
Office: CHL 103Mail Code: 0000 OTH

Education:
BS 1991 Microbiology - University of California, Los Angeles
PhD 1997 Micro & Molecular Genetics - University of California, Los angeles

Postdoctoral Research Fellowship:
1997-2000 Children's Hospital Los Angeles, California

Started at USC: 2000

Research Topics: Microbial/Invertebrate Genetics, Evolutionary Biology, Cardiovascular Disease, Immunology, Cellular Neurobiology

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Research Description

Neonatal Bacterial Sepsis and Meningitis

In my laboratory, we are dedicated to investigating the pathogenesis of neonatal bacterial invasive diseases. In particular we are examining the molecular basis by which E. coli K1, the most common gram-negative bacterium to cause bacterial sepsis and meningitis in the neonate, is able to translocate the gastric mucosa, disseminate to deeper tissues, cause bacteremia and penetrate the blood-brain barrier. We have made significant progress in this area. For example, we have discovered that E. coli K1 TraJ-dependent interactions with professional phagocytes play a critical role in the ability of this organism to disseminate to lymphoid tissues. The second area of research within my laboratory is investigating the molecular basis by which Citrobacter koseri are able to survive and intracellularly replicate within macrophages. C. koseri are unique from other neonatal meningitis causing organisms in that they have a very high propensity to cause brain abscess. We have made the novel observation that C. koseri, is capable of surviving phago-lysosomal fusion and replicating long-term within macrophages. Further, we have established the neonatal rat model of C. koseri brain abscess formation. Current work within our laboratory involves understanding the molecular basis for C. koseri to interact with macrophages and cause brain abscess. One of the most powerful tools that we have established in my laboratory is the biologically relevant neonatal rat model of bacterial disease. Using these models we are assessing the pathogenicity of the above mentioned organisms (and derived mutants) and to better understand colonization, gut translocation, systemic dissemination, bacteremia, and meningitis (E. coli K1 studies) and infection, meningitis, and brain abscess formation (Citrobacter spp. studies) and the specific role the host immune response plays in the disease process. These research endeavors will lead to improved knowledge regarding these devastating diseases and certainly assist in the development of enhanced diagnostics, therapeutics, and treatment strategies.

Selected Publications

Hill VT, Townsend SM, Arias RS, Jenabi JM, Gomez-Gonzalez I, Shimada H, Badger JL. - TraJ-dependent Escherichia coli K1 interactions with professional phagocytes are important for early systemic dissemination of infection in the neonatal rat. - Infect Immun [ 2004 ] Jan;72(1):478-88 . PubMed

Townsend SM, Pollack HA, Gonzalez-Gomez I, Shimada H, Badger JL. - Citrobacter koseri brain abscess in the neonatal rat: survival and replication within human and rat macrophages. - Infect Immun [ 2003 ] Oct;71(10):5871-80 . PubMed

Hoffman JA, Badger JL, Zhang Y, Kim KS. - Escherichia coli K1 purA and sorC are preferentially expressed upon association with human brain microvascular endothelial cells. - Microb Pathog [ 2001 ] Aug;31(2):69-79 . PubMed

Badger JL, Young BM, Darwin AJ, Miller VL. - Yersinia enterocolitica ClpB affects levels of invasin and motility. - J Bacteriol [ 2000 ] Oct;182(19):5563-71 . PubMed

Hoffman JA, Badger JL, Zhang Y, Huang SH, Kim KS. - Escherichia coli K1 aslA contributes to invasion of brain microvascular endothelial cells in vitro and in vivo. - Infect Immun [ 2000 ] Sep;68(9):5062-7 . PubMed

Badger JL, Wass CA, Weissman SJ, Kim KS. - Application of signature-tagged mutagenesis for identification of escherichia coli K1 genes that contribute to invasion of human brain microvascular endothelial cells. - Infect Immun [ 2000 ] Sep;68(9):5056-61 . PubMed

Young GM, Badger JL, Miller VL. - Motility is required to initiate host cell invasion by Yersinia enterocolitica. - Infect Immun [ 2000 ] Jul;68(7):4323-6 . PubMed

Badger JL, Wass CA, Kim KS. - Identification of Escherichia coli K1 genes contributing to human brain microvascular endothelial cell invasion by differential fluorescence induction. - Mol Microbiol [ 2000 ] Apr;36(1):174-82 . PubMed

Badger JL, Stins MF, Kim KS. - Citrobacter freundii invades and replicates in human brain microvascular endothelial cells. - Infect Immun [ 1999 ] Aug;67(8):4208-15 . PubMed

Badger JL, Kim KS. - Environmental growth conditions influence the ability of Escherichia coli K1 to invade brain microvascular endothelial cells and confer serum resistance. - Infect Immun [ 1998 ] Dec;66(12):5692-7 . PubMed


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