36 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

    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

    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

    Clustering.

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    <p>Hierarchal clustering according to Johnsons of phosphorylation states of whole lung lysates <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0018519#pone.0018519-Johnson1" target="_blank">[18]</a> (a). Venn diagram of spots phosphorylated at measured time points. 3 hours is depicted in blue, 6 hours in yellow, 24 hours in green and 48 hours in red (b). Kinase activities spanning multiple time points (intermediate colors) are listed.</p

    Early increase and later decrease in GSK-3β activity.

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    <p>Western blot of total GSK-3β and GSK-3β phosphorylation at ser9 (a: blot, b: quantification of phospho corrected for total GSK-3β). P-GSK-3β at Ser 9 inhibits phosphorylation of its substrate GS1 as depicted in Figure 5c. These data were derived from the kinomics chip. Data are presented as mean ± SD of n = 3.</p

    β-catenin levels decrease over time.

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    <p>Western blot (a) and quantification (b) of β-catenin. β-catenin protein levels decrease during <i>S. pneumoniae</i> pneumonia. Indirectly, represent a decrease of potentially active β-catenin. Data are represented as mean ± SD of n = 3.</p

    Provisional signal transduction scheme of active signaling pathways during pneumonia.

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    <p>Activation is depicted in green and inhibition in red, direction of events is calculated in relation to the noninfected control. Events from all timepoints (3, 6, 24 and 48 hours) were used to construct this scheme representing the entire host response dynamics of pneumococcal pneumonia. Important are the overall increment of chemotoxic stress and the initiation of the Th1 response. Spot numbers and activities (up ↑ or down ↓) are presented with corresponding kinases and timepoints. WNT signaling and the cell cycle are reduced throughout <i>S. pneumoniae</i> pneumonia.</p
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