Translate text to:
In JoVE (1)
Other Publications (2)
Articles by Lisa J. Ioannidis in JoVE
Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
Victoria Ryg-Cornejo1, Lisa J. Ioannidis1, Diana S. Hansen1
1The Walter and Eliza Hall Institute of Medical Research
A method for isolation of adherent inflammatory leukocytes from brain blood vessels of Plasmodium berghei ANKA-infected mice is described. The method allows quantification as well as phenotypic characterization of isolated leukocytes after staining with fluorescent antibodies and subsequent analysis by flow cytometry.
Published January 2, 2013. Keywords: Immunology, Infection, Infectious Diseases, Pathology, Hematology, Molecular Biology, Cellular Biology, Mouse, Brain, Intravascular inflammation, leukocytes, Plasmodium berghei, parasite, malaria, animal model, flow cytometry
Other articles by Lisa J. Ioannidis on PubMed
PloS One. 2011 | Pubmed ID: 21423798
Neutrophils have been implicated in both protective and pathological responses following influenza virus infections. We have used mAb 1A8 (anti-Ly6G) to specifically deplete LyG6(high) neutrophils and induce neutropenia in mice infected with virus strains known to differ in virulence. Mice were also treated with mAb RB6-8C5 (anti-Ly6C/G or anti-Gr-1), a mAb widely used to investigate the role of neutrophils in mice that has been shown to bind and deplete additional leukocyte subsets. Using mAb 1A8, we confirm the beneficial role of neutrophils in mice infected with virus strains of intermediate (HKx31; H3N2) or high (PR8; H1N1) virulence whereas treatment of mice infected with an avirulent strain (BJx109; H3N2) did not affect disease or virus replication. Treatment of BJx109-infected mice with mAb RB6-8C5 was, however, associated with significant weight loss and enhanced virus replication indicating that other Gr-1(+) cells, not neutrophils, limit disease severity during mild influenza infections.
Journal of Virology. May, 2012 | Pubmed ID: 22419813
The interaction between influenza virus and dendritic cells (DCs) remains poorly defined and controversial. Here we show that influenza virus replication in mouse bone marrow-derived DCs is abortive, despite viral genome transcription and replication occurring for each gene segment and viral hemagglutinin and nucleoprotein, at least, being produced. Electron microscopy reveals that virus assembly, rather than release of virus from the cell surface, is defective.