82 research outputs found

    Effect of MyD88 deficiency on total and differential lung cell counts.

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    <p>Total leukocyte counts (×10<sup>5</sup>/ml) and differential cell counts in lungs of wild-type (WT) and MyD88 knock-out mice 24 hours after intranasal infection with 5×10<sup>2</sup> CFU of <i>B. pseudomallei</i>. Data are mean±SEM (n = 6–7/group); ** <i>P</i><0.01 versus WT.</p

    MyD88 KO mice show increased bacterial outgrowth during experimental melioidosis.

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    <p>WT and MyD88 KO mice were intranasally infected with <i>B. pseudomallei</i> (5×10<sup>2</sup> CFU). Bacterial loads were measured 24 h and 72 h after inoculation in lungs (A), liver (B) and blood (C). Data are mean±SEM (n = 6–7 per group at each time point). ** <i>P</i><0.01.</p

    MyD88 KO, but not TRIF KO, mice show an accelerated mortality during experimental melioidosis.

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    <p>Survival of wild-type (WT, open rounds) and MyD88 KO mice (black squares) (A) or TRIF mutant (black squares) mice (B) intranasally infected with 5×10<sup>2</sup> CFU <i>B. pseudomallei</i>. Mortality was assessed twice daily for one week. n = 8–10 per group; ns denotes not significant; <i>P</i> value indicates the difference between MyD88 KO and WT mice.</p

    MyD88 plays an important role in early neutrophil recruitment after infection with <i>B. pseudomallei</i>.

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    <p>The impact of MyD88 deficiency on early neutrophil recruitment was investigated by analysing the amount of neutrophils in the pulmonary compartment using FACS analysis (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0003494#s2" target="_blank">Methods</a>) 24 h after intranasal inoculation of WT and MyD88 KO mice with 5×10<sup>2</sup> CFU <i>B. pseudomallei</i>. MyD88 KO mice displayed significantly fewer neutrophils in their lungs compared with WT mice (the percentages of neutrophils of the total pulmonary cell count are given from one respresentative WT and one respresentative MyD KO mouse) (A). Additionally, MyD88 deficient neutrophils (gray line and gray bars) present at t = 24 expressed less CD11b on their surface compared to WT neutrophils (black line and white bars): representative histograms show decreased CD11b expression on pulmonary neutrophils (B). This corresponded with lower MPO levels in lung homogenates of MyD88 KO mice (gray bars) compared to controls (white bars) (C). In line, pulmonary MIP-2 (D) and KC (E) levels tended to be lower or were significantly reduced in MyD88 KO mice. LIX levels were unaltered in MyD88 KO mice at this early time point (F). SSC, side scatter; FITC: fluorescein isothiocyanate; PE, phycoerythrin; MFI, mean fluorescence intensity; MPO, Myeloperoxidase; MIP-2: macrophage-inflammatory protein-2; LIX, lipopolysaccharide-induced CXC chemokine. Bar figures represent mean±SEM; n = 6–8 per mouse strain. * <i>P</i><0.05; ** <i>P</i><0.01.</p

    No difference in <i>B. pseudomallei</i> phagocytosis or killing capacity between WT and MyD88 KO cells.

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    <p>(A) Peripheral blood neutrophils were incubated at 37°C with CFSE-labeled growth-arrested <i>B. pseudomallei</i> (1×10<sup>7</sup> CFU/ml) after which time-dependent phagocytosis was quantified; 1×10<sup>4</sup> neutrophils were analysed per sample (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0003494#s2" target="_blank">Methods</a> section). (B) Killing capacity of peritoneal macrophages are shown as percentage of killed <i>B. pseudomallei</i> compared to t = 0. Data are mean±SEM; n = 5 per mouse strain. Open rounds represent WT cells, while black squares represent MyD88 KO mice; ns denotes not significant.</p

    ROC analyses, graphical representation.

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    <p>Receiver operating characteristic (ROC) analysis of urine sEPCR concentration for the prediction of ABMR in kidney transplantation. ROC analysis demonstrated that urinary sEPCR is appropriate to discriminate between ABMR patients and TCMR or control patients. In grey: ABMR vs. Control, in black: ABMR vs. TCMR.</p

    EPCR expression patterns in transplant biopsies.

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    <p>Representative immunostainings of kidney biopsies for EPCR in glomeruli (×32 magnification), peritubular capillaries (×64), arteries (×64), veins (×64) and tubules (x64). Arteries were always positive; therefore no picture with a score of 0 is shown. For tubules no score of 3 was assigned.</p

    EPCR mRNA expression in kidney transplant.

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    <p>EPCR mRNA levels were measured with qPCR on whole kidney biopsies. Results are shown as ratio between EPCR and HPRT Ct. Antibody-mediated (ABMR) rejection patients showed higher levels of EPCR mRNA than T-cell-mediated rejection (TCMR) patients. Results are shown as median, interquartile range and range. ** p<0.001 (Mann-Whitney Test)</p

    Clinical parameters of the included patients.

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    <p>Date are shown as median and range unless stated otherwise</p><p>a: p<0.05 (Mann-Whitney Test)</p>§<p>, *: p<0.001 (Mann-Whitney Test)</p

    sEPCR in serum (A) and urine (B) of transplant patients.

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    <p>Plasma and urine sEPCR concentration were measured with ELISA, urinary sEPCR concentration is corrected for the urine dilution by dividing the concentration by the urinary creatinine concentration. Plasma sEPCR levels did not differ. Urine sEPCR levels are elevated in the ABMR group than in patients with TCMR or without rejection. Results are shown as median, interquartile range and range. * p<0.01 (Mann-Whitney Test)</p
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