Brucella abortus rough mutants induce macrophage oncosis that requires bacterial protein synthesis and direct interaction with the macrophage.

Infection and Immunity
Jianwu PeiThomas A Ficht

Abstract

Previous studies suggest that smooth Brucella organisms inhibit macrophage apoptosis. In contrast, necrotic cell death of macrophages infected with rough Brucella organisms in vitro has been reported, which may in part explain the failure of some rough organisms to thrive. To characterize these potential macrophage killing mechanisms, J774.A1 murine macrophages were infected with Brucella abortus S2308-derived rough mutant CA180. Electron microscopic analysis and polyethylene glycol protection assays revealed that the cells were killed as a result of necrosis and oncosis. This killing was shown to be unaffected by treatment with carbenicillin, an inhibitor of bacterial cell wall biosynthesis and, indirectly, replication. In contrast, chloramphenicol treatment of macrophages infected at multiplicities of infection exceeding 10,000 prevented cell death, despite internalization of large numbers of bacteria. Similarly, heat-killed and gentamicin-killed CA180 did not induce cytopathic effects in the macrophage. These results suggested that killing of infected host cells requires active bacterial protein synthesis. Cytochalasin D treatment revealed that internalization of the bacteria was necessary to initiate killing. Transwell expe...Continue Reading

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Dec 11, 2008·Immunologic Research·Adam D Kennedy, Frank R DeLeo
Sep 18, 2007·Journal of Bacteriology·Gen-ichiro SanoKoichi Matsuo
Sep 11, 2009·International Journal of Biological Sciences·Xinglin ZhangQingmin Wu
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Mar 19, 2014·Frontiers in Cellular and Infection Microbiology·Jianwu PeiThomas A Ficht
Feb 12, 2019·Frontiers in Pharmacology·Johan Georg VisserCarine Smith
Feb 12, 2021·Microbiology and Molecular Biology Reviews : MMBR·R Martin RoopDaniel W Martin
Aug 3, 2021·Frontiers in Microbiology·Lauren W Stranahan, Angela M Arenas-Gamboa

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