44 research outputs found

    CpG-B-induced death of <i>R. australis</i>-infected mice is independent of pDC.

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    <p>Depletion of pDC was performed as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0034062#s2" target="_blank"><i>Methods</i></a>. At day 2 after infection with <i>R. australis</i> (5×10<sup>5</sup> pfu), 50 µg of CpG-B per mouse were injected i.v. into control or pDC-depleted mice. Mouse survival (6–8 mice per group) was monitored for 14 days.</p

    Treatment with CpG-B induced cell apoptosis through IDO.

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    <p>Apoptotic cells in spleen tissues at day 5 postinfection were detected by TUNEL assay (magnification ×20). Green (fluorescein) staining of apoptotic cells and blue (DAPI) staining of nuclei. Shown are the representative results from three independent experiments.</p

    Multiple intracellular cytokines produced by CD4<sup>+</sup> and CD8<sup>+</sup> T cells.

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    <p>At day 2 after infection with 5×10<sup>5</sup> pfu of <i>R. australis</i>, 50 µg of ODN control (ODN 1826 control) and CpG-B (ODN 1826) per mouse were injected i.v. into WT and IDO<sup>−/−</sup> mice (4 mice per group). At day 5 post-infection, spleen cells (1×10<sup>6</sup>/ml) from individual mice were restimulated with PMA/Ionomycin/GolgiStop for 5 h. Multiple intracellular cytokines as indicated were measured in CD4<sup>+</sup> and CD8<sup>+</sup> T cells. The percentages of intracellular cytokine production in gated T cells were shown as mean ± SD in the corner (A). Representative statistical data are shown from one of three independent experiments. * <i>p</i><0.05 (B).</p

    CpG-B treatment promotes T cell activation partially through IDO, without altering the frequencyof Treg cells.

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    <p>At day 5 post-infection, spleen cells from individual mice (4 mice per group) were stained with the indicated cell surface markers and then for intracellular Foxp3. Based on forward scatter (FSC) and side scatter (SSC) parameters, two populations were defined as quiescent cells (region 1, R1) and activated cells (region 2, R2) (A). The percentages of CD25<sup>+</sup> Foxp3<sup>+</sup> Treg cells and CD25<sup>+</sup> Foxp3<sup>−</sup> activated T cells gated in CD3<sup>+</sup> CD4<sup>+</sup> and CD3<sup>+</sup> CD8<sup>+</sup> T cells from R1 and R2 populations are shown as mean ± SD in the corner. Representative statistical data are shown from one of three independent experiments (B). * <i>p</i><0.05.</p

    NO is partially involved in CpG-B-induced death of <i>R. australis</i>-infected mice.

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    <p>WT and iNOS<sup>−/−</sup> mice (8 mice per group) were injected i.v. with different doses of <i>R. australis</i> (A). At day 2 after infection with 5×10<sup>5</sup> pfu of <i>R. australis</i>, 50 µg of ODN control (ODN 1826 control) and CpG-B (ODN 1826) per mouse were injected i.v. into WT and iNOS<sup>−/−</sup> mice (8 mice per group), respectively (B). Mouse survival was monitored for 14 days.</p

    CpG-B induced death of <i>R. australis</i>-infected mice through IDO.

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    <p>WT and IDO<sup>−/−</sup> mice (6–8 mice per group) were injected i.v. with different doses of <i>R. australis</i>. Mouse survival was monitored for 14 days (A). 50 µg of ODN control (ODN 1826 control) or CpG-B (ODN 1826) per mouse were injected i.v. into B6 and IDO<sup>−/−</sup> mice (8 mice per group) at day 2 after infection with 5×10<sup>5</sup> pfu of <i>R. australis</i>, respectively. Mouse survival was monitored for 14 days (B). Tissue bacterial loads determined by realtime PCR (C) and tissue IDO enzymatic activity determined by modified colorimetric assay (4 mice per group) were measured on day 5 post-infection (D). The representative results are shown as mean ± SD from three independent experiments. * <i>p</i><0.05.</p

    Treatment with CpG-B enhanced PD-1 expression on T cells partially through IDO.

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    <p>The percentages of PD-1 on CD4<sup>+</sup> and CD8<sup>+</sup> T cells that were gated on R1 and R2 CD3<sup>+</sup> T cells (as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0034062#pone-0034062-g005" target="_blank">Figure 5</a>) were determined by FACS at day 5 post-infection (A). The percentages of PD-1 expression in gated CD4<sup>+</sup> and CD8<sup>+</sup> T cells are shown as mean ± SD (B). Representative statistical data are shown from one of three independent experiments. * <i>p</i><0.05.</p

    CpG-B, not CpG-A, treatment induces mortality in otherwise sublethal rickettsial infection.

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    <p>B6 mice (8 mice per group) were injected i.v. with different doses of <i>R. australis</i> (<i>Ra</i>) (A). At day 2 after infection with 5×10<sup>5</sup> pfu of <i>R. australis</i>, 50 µg of ODN control (ODN 1826 control) and CpG-B (ODN 1826) per mouse were injected i.v., respectively (B). At day 2 after B6 mice (8 mice per group) were injected i.v. with <i>R. australis</i> (6×10<sup>5</sup> pfu), 50 µg of ODN control (ODN 1585 control), CpG-A (ODN 1585), and CpG-B (ODN 1826) per mouse were injected i.v., respectively (C). Survival was monitored for 14 days.</p

    Histopathological comparison of MHC I<sup>-/-</sup> mice and WT mice infected with <i>O</i>. <i>tsutsugamushi</i>.

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    <p>Foci of inflammation (arrows), including infiltration of macrophages and lymphocytes, were observed in infected mice (<b>A</b>, mag: 100x, 400x inset). Many apoptotic cells, possibly neutrophils, were observed in the liver of MHC I<sup>-/-</sup> mice. Increased necrosis and steatosis (arrows with circle end) were observed in the livers of MHC I<sup>-/-</sup> mice. Higher pathology scores indicating greater injury were observed in the livers of infected mice (<b>B</b>). There were significantly more apoptotic cells in the liver (<b>C</b>) and kidney (<b>D</b>) of MHC I<sup>-/-</sup> mice than their WT counterparts. All infected mice had increased apoptosis compared to uninfected mice. *, p<0.05; ***, p<0.001, n = 8; each tissue sample was blindly scored by four experienced investigators.</p

    Survival and bacterial loads of MHC I<sup>-/-</sup> mice and WT mice infected with <i>O</i>. <i>tsutsugamushi</i>.

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    <p>All infected MHC I<sup>-/-</sup> mice (open circles) became moribund between 10 and 12 dpi while none of the infected WT mice (solid circles) expired (<b>A</b>). MHC I<sup>-/-</sup> mice had significantly greater bacterial loads in the lung, liver, kidney, and spleen than in the WT mice at 11 dpi (<b>B</b>). *, p<0.05; n = 8.</p
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