19 research outputs found

    NOD2 deficiency reduces the capacity of alveolar macrophages and neutrophils to internalize <i>S</i>. <i>pneumoniae in vitro</i>.

    No full text
    <p>Growth arrested, FITC labeled <i>S</i>. <i>pneumoniae</i> D39 were incubated with alveolar macrophages (A) or CFSE-labeled <i>S</i>. <i>pneumoniae</i> D39 with peripheral blood neutrophils (B) from wild-type (Wt) and <i>Nod2</i><sup><i>−/−</i></sup> mice at 4°C (n = 3–4 per mouse strain) or 37°C (n = 6–8 per mouse strain) for 1 hour after which phagocytosis was quantified. Data are expressed as box-and-whisker diagrams depicting the smallest observation, lower quartile, median, upper quartile and largest observation; *<i>P</i><0.05, ***<i>P</i><0.001 versus Wt cells.</p

    Cytokine and chemokine concentrations in lung homogenates of wild-type and <i>Nod2</i><sup><i>-/-</i></sup>mice during pneumococcal pneumonia caused by serotype 2 <i>S</i>. <i>pneumoniae</i> (D39).

    No full text
    <p>Proinflammatory cytokine (TNF-α, IL-1β, IL-6) and chemokine (KC, MIP-2 and CCL2) levels in lung homogenates at 6, 24 and 48 hours after intranasal <i>S</i>. <i>pneumoniae</i> D39 infection in wild-type (Wt) and <i>Nod2</i><sup><i>-/-</i></sup> mice. Data are expressed as box-and-whisker diagrams depicting the smallest observation, lower quartile, median, upper quartile and largest observation (8 mice per group at each time point); * <i>P</i><0.05, ** <i>P</i><0.01.</p

    NOD2 deficiency results in defective pulmonary clearance of non-encapsulated mutant <i>S</i>. <i>pneumoniae</i> D39Δ<i>cps</i>.

    No full text
    <p>Wild-type (Wt) and <i>Nod2</i><sup><i>−/−</i></sup> mice were intranasally infected with 10<sup>8</sup> CFU of <i>S</i>. <i>pneumoniae</i> D39Δ<i>cps</i> and sacrificed 6 or 24 hours later. Bacterial loads were determined in lung homogenates. Data are expressed as box-and-whisker diagrams depicting the smallest observation, lower quartile, median, upper quartile and largest observation (8 mice per group at each time point); * <i>P</i><0.05.</p

    Cytokine and chemokine concentrations in lung homogenates of wild-type (Wt) and <i>Nod2</i><sup><i>-/-</i></sup> mice during pneumococcal pneumonia caused by an unencapsulated mutant strain serotype 2 <i>S</i>. <i>pneumoniae</i> D39Δ<i>cps</i>.

    No full text
    <p>Proinflammatory cytokine (TNF-α, IL-1β, IL-6) and chemokine (KC, MIP-2 and CCL2) levels in lung homogenates at 6 and 24 hours after intranasal <i>S</i>. <i>pneumoniae</i> D39Δ<i>cps</i> infection in wild-type (Wt) and <i>Nod2</i><sup><i>-/-</i></sup> mice. Data are expressed as box-and-whisker diagrams depicting the smallest observation, lower quartile, median, upper quartile and largest observation (8 mice per group at each time point); * <i>P</i><0.05.</p

    NOD2 deficiency does not influence lung pathology and neutrophil recruitment during pneumonia caused by serotype 2 <i>S</i>. <i>pneumoniae</i> (D39).

    No full text
    <p>Wild-type (Wt) and <i>Nod2</i><sup><i>−/−</i></sup> mice were intranasally infected with 10<sup>7</sup> CFU of <i>S</i>. <i>pneumoniae</i> D39 and sacrificed 6, 24 or 48 hours later. Representative hematoxylin and eosin (HE) stainings of lung tissue of Wt (A) and <i>Nod2</i><sup><i>-/-</i></sup> mice (B) 24 hours after inoculation with <i>S</i>. <i>pneumoniae</i> D39 (original magnification ×200). Quantification of pulmonary Ly-6G positivity (F) and MPO levels in whole lung homogenates (G) 6, 24 or 48 hours after intranasal infection with <i>S</i>. <i>pneumoniae</i> D39 of wild-type (Wt) and <i>Nod2</i><sup><i>−/−</i></sup> mice. Representative neutrophil stainings (brown) of Wt (D) and <i>Nod2</i><sup><i>−/−</i></sup> mice (E) 24 hours after induction of pneumococcal pneumonia are shown (original magnification ×200). Data are expressed as box-and-whisker diagrams depicting the smallest observation, lower quartile, median, upper quartile and largest observation (8 mice per group at each time point). Differences between groups were not significant.</p

    NOD2 deficiency does not influence lung pathology and neutrophil recruitment during pneumonia caused by an unencapsulated mutant <i>S</i>. <i>pneumoniae</i> D39Δ<i>cps</i>.

    No full text
    <p>Wild-type (Wt) and <i>Nod2</i><sup><i>−/−</i></sup> mice were intranasally infected with 10<sup>8</sup> CFU of <i>S</i>. <i>pneumoniae</i> D39Δ<i>cps</i> and sacrificed 6 or 24 hours later. Representative hematoxylin and eosin (HE) stainings of lung tissue of Wt (A) and <i>Nod2</i><sup><i>-/-</i></sup> mice (B) 24 hours after inoculation with <i>S</i>. <i>pneumoniae</i> (original magnification ×200). Quantification of pulmonary Ly-6G positivity (F) and MPO levels in whole lung homogenates (G) 6 or 24 hours after intranasal infection with <i>S</i>. <i>pneumoniae</i> D39Δ<i>cps</i> of wild-type (Wt) and <i>Nod2</i><sup><i>−/−</i></sup> mice. Representative neutrophil stainings (brown) of Wt (D) and <i>Nod2</i><sup><i>−/−</i></sup> mice (E) 24 hours after induction of pneumococcal pneumonia are shown (original magnification ×200). Data are expressed as box-and-whisker diagrams depicting the smallest observation, lower quartile, median, upper quartile and largest observation (8 mice per group at each time point). Differences between groups were not significant.</p

    Effect of TREM-1 deficiency on bacterial clearance, pulmonary neutrophil influx and organ damage during experimental melioidosis.

    No full text
    <p>WT (closed circles/black bars) and <i>Trem-1/3</i><sup><i>-/-</i></sup> mice (open circles/ white bars) were intranasally infected with 5 x 102 CFU of <i>B</i>. <i>pseudomallei</i> and sacrificed 24 and 72 h post-infection, followed by determination of bacterial loads in lung homogenate <b>(</b><i>A</i><b>),</b> BALF <b>(</b><i>B</i><b>),</b> blood <b>(</b><i>C</i><b>)</b> and liver <b>(</b><i>D</i><b>).</b> Neutrophil influx as determined by % Ly6G positive surface of lung slides was calculated for WT and <i>Trem-1/3</i><sup><i>-/-</i></sup> mice <b>(</b><i>E</i><b>).</b> Lung <b>(</b><i>F</i><b>)</b> and spleen <b>(</b><i>G</i><b>)</b> pathology was scored as described in the Methods section. Aspartate transaminase (AST; <i>H</i><b>),</b> alanine transaminase (ALT; <i>I</i>), lactate dehydrogenase (LDH; <i>J</i><b>)</b> and blood urea nitrogen (BUN; <i>K</i>) were measured as a marker for end organ damage. Data are expressed as mean ± SEM. n = 7–8 mice per group. *<i>P</i> < 0.05; **<i>P</i>< 0.01 (Mann-Whitney <i>U</i> test).</p

    Reduced neutrophil influx in lungs of <i>Trem-2</i> <sup><i>-/-</i></sup> mice, without affecting lung pathology.

    No full text
    <p>Lung pathology was determined in wild-type (WT; black bars) and <i>Trem-2</i><sup><i>-/-</i></sup> mice (white bars) infected with 5 x 102 CFU <i>B</i>. <i>pseudomallei</i> at 72h post-infection as described in the Methods section (<i>A</i>). Representative lung slides of WT (<i>B</i>) and <i>Trem-2</i><sup><i>-/-</i></sup> mice (<i>C</i>) (original magnification 10x). Neutrophil influx was defined by Ly6G positivity (expressed as % of total lung surface; <i>D</i>). Representative photographs of Ly6G-immunostaining for granulocytes on lung slides of WT (<i>E</i>) and <i>Trem-2</i><sup><i>-/-</i></sup> mice (<i>F</i>) (original magnification 10x). Data are expressed as mean ± SEM, n = 5–6 mice per group per time point. * <i>P</i> < 0.05. (Mann-Whitney <i>U</i> test).</p

    No effect of TREM-1 deficiency on the cellular responsiveness and phagocytosis or intracellular killing of <i>B</i>. <i>pseudomallei</i>.

    No full text
    <p>Whole blood (<i>A</i>), bone marrow derived macrophages (BMDM; <i>B</i>) and alveolar macrophages (AM; <i>C</i><b>)</b> of WT and <i>Trem-1/3</i><sup><i>-/-</i></sup> mice were stimulated with medium, <i>E</i>.<i>coli</i> LPS(100 ng/ml) or heat-inactivated wild type <i>B</i>. <i>pseudomallei</i> (107 CFU/ml at a MOI of 50). TNF-α levels were measured in the supernatant obtained after 20 h of stimulation. BMDM (<i>D</i>) and AM (<i>E</i>) of WT and <i>Trem-1/3</i><sup><i>-/-</i></sup> mice were incubated at 37°C with FITC labeled heat-inactivated <i>B</i>. <i>pseudomallei</i> after which time-dependent phagocytosis was determined. Data are expressed as mean ± SEM and are representative of two or three independent experiments. n = 4 or 8 (for the whole blood assay) per group. *<i>P</i>< 0.05 (Mann-Whitney <i>U</i> test).</p
    corecore