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Results: 7

1.
Figure 7

Figure 7. From: Pulmonary inflammation induced by subacute ozone is augmented in adiponectin deficient mice: role of IL-17A.

IκBζ expression is increased in adiponectin deficient mice. IκBζ mRNA normalized to 18S in adiponectin deficient (Adipo−/−) and wildtype mice exposed to room air or ozone (0.3ppm) for 24 or 48 hours. # p<0.05 vs wildtype mice with same exposure, n=3 per group for air exposure, and n=5–7 per group for ozone exposure.

David I. Kasahara, et al. J Immunol. ;188(9):4558-4567.
2.
Figure 6

Figure 6. From: Pulmonary inflammation induced by subacute ozone is augmented in adiponectin deficient mice: role of IL-17A.

Numbers of IL-17 producing macrophages and γδ T cells. (A) IL-17 producing interstitial macrophages (F4/80+ and CD11c) in the lung. (B) Total γδ T cells and (C) IL-17A producing (after PMA plus ionomycin stimulation) γδ T cells. Data are expressed as mean±SEM. * p<0.05 (air vs ozone exposed mice of same genotype) ; # p<0.05 (Adipo−/− vs wildtype mice with ozone exposure). n=6 in each group.

David I. Kasahara, et al. J Immunol. ;188(9):4558-4567.
3.
Figure 3

Figure 3. From: Pulmonary inflammation induced by subacute ozone is augmented in adiponectin deficient mice: role of IL-17A.

Ozone induced inflammatory markers are increased in adiponectin deficient mice (A-G). Cytokines and chemokines in bronchoalveolar lavage (BAL) fluid of adiponectin deficient (Adipo−/−) or wildtype mice exposed to air or ozone (0.3 ppm for 72 h). *p<0.05 vs genotype matched air exposed mice, # p<0.05 vs exposure matched wildtype mice. All data are expressed as mean±SEM. N= 4–7 per group.

David I. Kasahara, et al. J Immunol. ;188(9):4558-4567.
4.
Figure 2

Figure 2. From: Pulmonary inflammation induced by subacute ozone is augmented in adiponectin deficient mice: role of IL-17A.

Ozone induced inflammation is increased in adiponectin deficient mice. Bronchoalveolar lavage (BAL) neutrophils (A), macrophages (B), and protein (an index of lung injury) (C) in wildtype and adiponectin deficient (Adipo−/−) mice exposed to air or 0.3 ppm of ozone for 24, 48, or 72 hours. *p<0.05 versus genotype matched air exposed mice. # p<0.05 versus exposure matched wildtype mice. Data indicate mean±SEM. n=6–10 per group.

David I. Kasahara, et al. J Immunol. ;188(9):4558-4567.
5.
Figure 1

Figure 1. From: Pulmonary inflammation induced by subacute ozone is augmented in adiponectin deficient mice: role of IL-17A.

Adiponectin levels in serum and broncholalveolar lavage (BAL) fluid, and adiponectin isoform distribution in BAL. (A) Serum or (B) BAL adiponectin from air and subacute ozone (0.3ppm for 72 hrs) exposed wildtype mice quantified by ELISA. (C) Time course of adiponectin measured in the BAL of wildtype mice exposed to air and ozone at 12, 24 and 48 hours. (D) Adiponectin isoform distribution in BAL from air and subacute ozone exposed wildtype mice. Equal amounts of BAL fluid were loaded in each lane. Data expressed in mean±SEM. N=3 per group.

David I. Kasahara, et al. J Immunol. ;188(9):4558-4567.
6.
Figure 4

Figure 4. From: Pulmonary inflammation induced by subacute ozone is augmented in adiponectin deficient mice: role of IL-17A.

Ozone induced neutrophil recruitment in Adipo−/− mice is IL-17A dependent. (A) IL-17 mRNA expression normalized to 18S in adiponectin deficient (Adipo−/−) and wildtype mice exposed to room air or ozone (0.3ppm) for 24 or 48 hours. *p<0.05, air vs ozone exposed mice of same genotype; # p<0.05 wildtype vs Adipo−/− mice with same exposure, n= 3 per group for air exposure, and n=5–7 per group for ozone exposure. (B-H) Effect of anti-IL-17A (α IL-17 Ab) or isotype control antibody (Isotype Ab) on BAL neutrophils (B), protein (C), macrophages (D), IL-6 (E), KC (F), LIX (G), and G-CSF (H) in wildtype or Adipo−/− mice exposed to ozone (0.3 ppm) for 48 h. Data are expressed as mean±SEM. * p<0.05 versus wildtype mice with same antibody treatment; # p<0.05 versus genotype matched mice treated with control antibody

David I. Kasahara, et al. J Immunol. ;188(9):4558-4567.
7.
Figure 5

Figure 5. From: Pulmonary inflammation induced by subacute ozone is augmented in adiponectin deficient mice: role of IL-17A.

F4/80+CD11c macrophages and γδ T cells produce IL-17. (A) Adiponectin deficient (Adipo−/−) and wildtype mice exposed to room air or ozone (0.3ppm) for 72 hours. IL-17A expression in lung cells was identified by intracellular cytokine staining after gating on anti-CD45 positive cells. Numbers in the lower right hand corner indicate the % of CD45+IL-17+ cells in the lung. Bar graphic on right side indicates mean±SEM of CD45+IL17+ cells from lung cells suspension (n=6 per group, * p<0.05 air vs ozone, #p<0.05, wildtype vs Adipo−/− mice). (B) Hematopoietic cells were identified by CD45 staining, and alveolar macrophages (F4/80+ and CD11c+) or interstitial macrophages (F4/80+ and CD11c) were further analyzed for IL-17A expression. Shaded: isotype control, blue line is air exposure and red line is ozone exposure. (C) γδ T cells were identified using CD3 and TCRδ antibodies. IL-17A expression was examined in γδ T cells incubated for 5 hours with or without PMA and ionomycin (P+ I) stimulation. The right corner of figure 5C is a pseudo-density plot of IL17+ γδ T-cells.

David I. Kasahara, et al. J Immunol. ;188(9):4558-4567.

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