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The live vaccine strain of Francisella tularensis replicates in human and murine macrophages but induces only the human cells to secrete proinflammatory cytokines
Author(s) -
Bolger Courtney E.,
Forestal Colin A.,
Italo Jaime K.,
Benach Jorge L.,
Furie Martha B.
Publication year - 2005
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1104637
Subject(s) - francisella tularensis , proinflammatory cytokine , biology , chemokine , microbiology and biotechnology , tularemia , secretion , tumor necrosis factor alpha , monocyte , interleukin 8 , immunology , cytokine , immune system , virology , inflammation , virulence , biochemistry , gene
Francisella tularensis is the highly infectious agent of tularemia, a disease that can prove fatal in humans. An attenuated live vaccine strain (LVS) of this bacterium is avirulent in man but produces lethal illness in mice. As a step toward understanding the species specificity of the LVS, we compared its interactions with murine and human leukocytes. The bacterium replicated within murine bone marrow‐derived macrophages (muBMDM), human monocyte‐derived macrophages (huMDM), and freshly isolated human monocytes. However, the murine and human phagocytes differed in their ability to secrete proinflammatory cytokines in response to the LVS. The huMDM released large amounts of CXC chemokine ligand 8 (CXCL8) and CC chemokine ligand 2 when incubated with live or killed LVS organisms, and live bacteria also elicited production of interleukin‐1β (IL‐1β). Furthermore, human monocytes secreted CXCL8, IL‐1β, and tumor necrosis factor α in response to various bacterial preparations. In contrast, muBMDM produced little to no proinflammatory cytokines or chemokines when treated with any preparations of the LVS. Clearly, human and murine macrophages support growth of this bacterium. However, the greater proinflammatory response of human leukocytes to F. tularensis LVS may contribute to the avirulence of this strain in the human host.