18 research outputs found
MOESM3 of Blue light induces a neuroprotective gene expression program in Drosophila photoreceptors
Additional file 3: Table 2. GO term analysis of differentially regulated genes
MOESM1 of Blue light induces a neuroprotective gene expression program in Drosophila photoreceptors
Additional file 1: Fig. S1. The blue light treatment conditions used for RNA-seq analysis do not induce retinal degeneration. Fig. S2. Affinity-enrichment of photoreceptor nuclear RNA from day one dark-treated flies. Fig. S3. Newly-eclosed flies do not show any unique blue light-induced gene expression changes. Fig. S4. Promoter motifs enriched at blue light-regulated genes. Fig. S5. Distribution of promoter motifs in blue light-regulated genes
MOESM5 of Blue light induces a neuroprotective gene expression program in Drosophila photoreceptors
Additional file 5: Table 4. Fly stocks used in this study
MOESM2 of Blue light induces a neuroprotective gene expression program in Drosophila photoreceptors
Additional file 2: Table 1. Significantly differentially expressed genes identified under each comparison
MOESM4 of Blue light induces a neuroprotective gene expression program in Drosophila photoreceptors
Additional file 4: Table 3. Transcription factors matches for all motifs identified for blue light-regulated genes
Chlamydial Lung Infection Induces Transient IL-9 Production Which Is Redundant for Host Defense against Primary Infection
<div><p>IL-9/Th9 responses are recently found to be important for innate and adaptive immunity particularly in parasitic infections. To date, the study on the role of IL-9 in bacterial infections is limited and the reported data are contradictory. One reported function of IL-9/Th9 is to modulate Th1/Th17 responses. Since our and others’ previous work has shown a critical role of Th1 and Th17 cells in host defense against chlamydial lung infection, we here examined the role of IL-9 responses in <i>Chlamydia muridarum</i> (Cm) lung infection, particularly its effect on Th1 and Th17 responses and outcome infection. Our data showed quick but transient IL-9 production in the lung following infection, peaking at day 3 and back to baseline around day 7. CD4+ T cell was the major source of IL-9 production in the lung infection. Blockade of endogenous IL-9 using neutralizing antibody failed to change Interferon-γ (IFN-γ) and IL-17 production by cultured spleen mononuclear cells isolated from Cm infected mice. Similarly, in vivo neutralization of IL-9 failed to show significant effect on T cell (Th1 and Th17) and antibody responses (IgA, IgG1 and IgG2a). Consistently, the neutralization of IL-9 had no significant effect on disease process, including body weight change, bacterial burden and histopathological score. The data suggest that IL-9 production following chlamydial lung infection is redundant for host defense against the intracellular bacteria.</p></div
Kinetics of local IL-9, IL-17 and IFN-γ production following lung Cm infection. C57BL/6 Mice were inoculated intranasally with Cm (1×10<sup>3</sup> IFUs) and were sacrificed at the indicated days.
<p>The lungs were isolated and the lung homogenates was prepared to detect IL-9(A), IL-17(B) and IFNγ (C) protein levels by ELISA. One representative experiment of two independent experiments (4 mice in each group) is shown. The results are shown as mean ± SD. The levels of IL-9, IL-17 and IFN-γ at various days post-infection were compared to those on day 0 by ANOVA (*p<0.05;**p<0.01).</p
Intranasal delivery of anti-IL-9 mAb successfully neutralized IL-9 in the lung.
<p>C57BL/6 mice were intranasally administered with 10μg of either anti-mouse IL-9 mAb or isotype control antibody at day -1 (one day before), day 0, day 2 following Cm (1×10<sup>3</sup> IFUs) lung infection. On day 3 post-infection, mice were sacrificed and lung homogenates were prepared to detect IL-9 protein by ELISA. One representative experiment of two independent experiments (four mice in each group in each experiment) is shown. The results are shown as mean ± SD (**, p<0.01).</p
Production of IL-9 by lung mononuclear cells following Cm infection. Mice were inoculated intranasally with Cm (1×10<sup>3</sup> IFUs) and were sacrificed at day 3 post-infection.
<p>The isolated lung mononuclear cells were detected for IL-9 expression by FACS. (A) Representative intracellular IL-9 staining of CD45+ cells and absolute number of IL9 producing CD45+ cells in the lung. (B) Representative intracellular IL-9 staining and absolute number of IL-9 producing CD4+ (CD4+CD3+) T cells, CD8+ (CD8+CD3+) T cells, NK (NK1.1+CD3-) cells and NKT (CD1d tetramer+NK1.1+) cells in the lung. One representative experiment of two independent experiments (four mice in each group in each experiment) is shown. The results are shown as mean ± SD (*, p<0.05).</p
The neutralization of endogenous IL-9 has significant impact on infection process and histopathology in the lung.
<p>C57BL/6 mice were intranasally administered with 10μg of either anti-mouse IL-9 mAb or isotype control antibody at one day before and the same day of infection following by every 2 days thereafter. Mice were inoculated intranasally with 1×10<sup>3</sup> IFUs of Cm EBs. (A) The percentage of body weight changes in the two groups of mice. (B) Live chlamydial organisms (IFUs) in the lung on day 7 and day 14 after infection in each group. (C) The lung tissue sections from different experiment groups were tained with H&E and observed under light microscopy. (D) Semi-quantitative analysis of lung inflammation and damage (pathological score). Slides were examined by a blinded pathologist and the inflammatory grades were analyzed as described in Materials and Methods. One representative experiment of three independent experiments (four mice in each group in each experiment) is shown. The results are shown as mean ± SD.</p