Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Poly(ADP-ribose) polymerase-1 inhibition prevents eosinophil recruitment by modulating Th2 cytokines in a murine model of allergic airway inflammation: a potential specific effect on IL-5.

doi: 10.4049/jimmunol.177.9.6489

Figure Lengend Snippet: FIGURE 2. Effect of PARP-1 inhibition on eosinophil infiltration into airways and IgE production upon OVA sensitization and challenge. Mice were sensitized to and challenged with aerosolized OVA as described in Fig. 1. Mice were sacrificed 48 h after challenge and then subjected to BAL. A, BAL fluids were collected and centrifuged; cells were then dif- ferentially stained, and eosinophils were counted. The percentages at top of the different bars represent the eosinophils from total cell number collected by BAL. Mice were sacrificed 24 h after challenge and then subjected to BAL. B, BAL fluids were tested for IgE levels (nanogram per milliliter) by ELISA. Data are the mean SD of values from at least six mice per group. , p 0.01 difference from unchallenged mice; #, p 0.01 difference from wild-type mice challenged with OVA.

Article Snippet: Cells were seeded in triplicates at a density of 107 cells/ml after which they were either incubated with medium alone or exposed to 200 ng/ml OVA for 72 h. For the phenotype reversal, lung cell suspensions derived from OVA-challenged PARP-1 / mice were rechallenged with 200 ng/ml OVA in the presence or absence of recombinant mouse IL-5 (BD Pharmingen), IL-4 (BD Biosciences), or OVA-specific IgE (Serotec) at 100 ng/ml.

Techniques: Inhibition, Staining, Enzyme-linked Immunosorbent Assay

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Poly(ADP-ribose) polymerase-1 inhibition prevents eosinophil recruitment by modulating Th2 cytokines in a murine model of allergic airway inflammation: a potential specific effect on IL-5.

doi: 10.4049/jimmunol.177.9.6489

Figure Lengend Snippet: FIGURE 6. Effects of IL-5, IL-4, or IgE replenishment on GM-CSF production by PARP-1/ lung cells and on eosinophil-recruitment into airways of OVA-sensitized and OVA-challenged PARP-1/ mice. C57BL/6 PARP-1/ mice were sensitized to and challenged with OVA. Lung cells were isolated 24 h after challenge and then incubated with OVA in the absence or presence of IL-5, IL-4, or IgE for 72 h. Control cells were incubated in complete medium alone. A, GM-CSF expression (picogram per milliliter) was measured using the Bio-Rad Bioplex system. B, Effect of IL-4 replenishment on IL-5 production by lung cells derived from OVA-sensitized and challenged PARP-1/ mice. Lung cells were incubated with OVA or IL-4 or left untreated. IL-5 production was measured (picogram per milliliter) after a 72-h incubation. Data are given as the mean SD of values from at least six mice per group. #, p 0.01 difference from lung cells derived from OVA-challenged PARP-1/ mice that were restimulated with OVA in vitro. C–E, PARP-1/ mice were sensitized to and challenged with OVA. Twenty-four hours later, mice were subjected to intranasal administration of recombinant mouse IL-5, IL-4, or OVA-specific IgE. Mice were sacrificed 48 h after OVA challenged. The mice were then subjected to BAL or their lungs were fixed and analyzed histologically. C, Eosinophils were counted in BAL fluid. Data are given as the mean SD of values from at least five mice per group. Percentages shown on top of the different bars represent eosinophils from the total cell number collected by BAL. , p 0.01 difference from OVA-challenged PARP-1/

Article Snippet: Cells were seeded in triplicates at a density of 107 cells/ml after which they were either incubated with medium alone or exposed to 200 ng/ml OVA for 72 h. For the phenotype reversal, lung cell suspensions derived from OVA-challenged PARP-1 / mice were rechallenged with 200 ng/ml OVA in the presence or absence of recombinant mouse IL-5 (BD Pharmingen), IL-4 (BD Biosciences), or OVA-specific IgE (Serotec) at 100 ng/ml.

Techniques: Isolation, Incubation, Control, Expressing, Derivative Assay, In Vitro, Recombinant