Postdoctoral Fellow Yoon-Suk Kang's Brucella chemical genetics screen early release today in Infection and Immunity
Congratulations to Yoon-Suk on his latest Brucella neotomae manuscript: "A chemical genetics screen reveals influence of p38 map kinase and autophagy on phagosome development and intracellular replication of Brucella neotomae in macrophages"
Congratulations to postdoctoral fellow, Yoon-Suk Kang, on acceptance of his manuscript in Infection and Immunity. The manuscript is titled: "Brucella neotomae recapitulates attributes of zoonotic human disease in a murine infection model." One of my favorite figures are images of tdTomato-labeled Brucella detected by confocal microscopy replicating in the middle of a liver granulomas visualized by counterstaining with H&E. In contrast to wild type organisms, virB4 mutant bacteria are found as single cells in sinusoids presumably within Kuffpfer cells. Wild type bacteria are found at high levels in mouse thymus at all time points examined; virB4 mutant bacteria are undetectable in thymus. B. neotomae induces a Th-1 immune response. More information in the manuscript.
Image from lab meeting! Spinning disk confocal microscope image of B. neotomae and J744A.1 macrophages
Spinning disc confocal microscopy image acquired by Lucius Chiaraviglio and presented at Lab Meeting this past Friday. A single multiply infected macrophage is shown. Red objects are individual Brucella neotomae bacteria. Green immunofluorescent staining lables LAMP-1, a marker of late endosomes and lysosomes. Brucella traffics to LAMP-1 compartments early during infection.
Congratulations to Postdoctoral Fellow Yoon-Suk Kang on publication of his manuscript "Promotion and Rescue of Intracellular Brucella neotomae Replication During Co-Infection With Legionella pneumophila"
Published online today in Infection and Immunity: "Promotion and Rescue of Intracellular Brucella neotomae Replication During Co-Infection With Legionella pneumophila." Yoon-Suk created a versatile bioreporter toolkit to enable analysis of the fate of individual pathogens in polymicrobial infections. He then validated a type IV secretion system-dependent Brucella model using the wood rat pathogen, Brucella neotomae. In contrast to wild type organisms, Brucella T4SS mutants were completely defective in their ability to growth inside of macrophages. Fascinatingly co-infection with Legionella pneumophila, another T4SS-dependent pathogen, was able to rescue intracellular growth of the T4SS-mutant Brucella and also stimulated growth of wild type Brucella organisms! This was a one way rescue: Legionella could rescue Brucella, but wild type Brucellla could not rescue T4SS-defective Legionella.
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