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Results: 9

1.
Fig. 9.

Fig. 9. From: Human apolipoprotein E genotypes differentially modify house dust mite-induced airway disease in mice.

Summary of airway responses to repeated HDM challenges in humanized apoE knockin mice.

Xianglan Yao, et al. Am J Physiol Lung Cell Mol Physiol. 2012 January 15;302(2):L206-L215.
2.
Fig. 5.

Fig. 5. From: Human apolipoprotein E genotypes differentially modify house dust mite-induced airway disease in mice.

Effect of huApoE alleles on serum IgE levels in HDM-challenged mice. Quantification of serum IgE levels. (n = 19–20, *P < 0.001, huApoE + HDM vs. muApoE + HDM). Results are pooled from 2 experiments.

Xianglan Yao, et al. Am J Physiol Lung Cell Mol Physiol. 2012 January 15;302(2):L206-L215.
3.
Fig. 8.

Fig. 8. From: Human apolipoprotein E genotypes differentially modify house dust mite-induced airway disease in mice.

Expression of huApoE in the lungs of humanized apoE ε2, ε3, and ε4 mice. Lung protein expression of huApoE by humanized apoE ε2, ε3, and ε4 mice was assessed by Western blotting using an antibody directed against huApoE. Equivalency of protein loading was assessed using an antibody directed against β-actin. (n = 3 mice, *P < 0.001, huApoE2 + saline vs. huApoE3 + saline or huApoE4 + saline and huApoE2 + HDM vs. huApoE3 + HDM or huApoE4 + HDM). Duplicate samples are shown.

Xianglan Yao, et al. Am J Physiol Lung Cell Mol Physiol. 2012 January 15;302(2):L206-L215.
4.
Fig. 7.

Fig. 7. From: Human apolipoprotein E genotypes differentially modify house dust mite-induced airway disease in mice.

HDM-challenged humanized apoE ε3 mice have attenuated expression of lung chemokines. Quantification of lung mRNA levels for CCL11, CCL24, CCL7, and CCL17 by qRT-PCR presented as relative mRNA expression (n = 6 mice, *P < 0.05, huApoE + HDM vs. muApoE + HDM). Results are representative of 2 independent experiments.

Xianglan Yao, et al. Am J Physiol Lung Cell Mol Physiol. 2012 January 15;302(2):L206-L215.
5.
Fig. 6.

Fig. 6. From: Human apolipoprotein E genotypes differentially modify house dust mite-induced airway disease in mice.

Expression of lung Th2 and Th17 cytokines are decreased in HDM-challenged humanized apoE ε3 mice. Quantification of lung mRNA levels for IL-4, IL-13, IL-17A, and IL-10 by qRT-PCR presented as relative mRNA expression (n = 6 mice, *P < 0.05, huApoE + HDM vs. muApoE + HDM). Results are representative of 2 independent experiments.

Xianglan Yao, et al. Am J Physiol Lung Cell Mol Physiol. 2012 January 15;302(2):L206-L215.
6.
Fig. 4.

Fig. 4. From: Human apolipoprotein E genotypes differentially modify house dust mite-induced airway disease in mice.

HDM-induced airway inflammation is attenuated in humanized apoE ε3 mice. Numbers of total cells (A) and inflammatory cell types (B–E) present in bronchoalveolar lavage fluid (BALF) (n = 10 mice, *P < 0.05, huApoE + HDM vs. muApoE + HDM). Results are representative of 2 independent experiments.

Xianglan Yao, et al. Am J Physiol Lung Cell Mol Physiol. 2012 January 15;302(2):L206-L215.
7.
Fig. 3.

Fig. 3. From: Human apolipoprotein E genotypes differentially modify house dust mite-induced airway disease in mice.

Pathological manifestations of HDM-induced airway inflammation and mucous cell metaplasia are attenuated in humanized apoE ε3 mice. Histological sections of lung were stained with hematoxylin and eosin (H & E) or PAS stains and images obtained at ×200 or ×1,000. Calibration bars indicate 100 μm for the ×200 images and 20 μm for the ×1,000 images. Results are representative of 2 independent experiments.

Xianglan Yao, et al. Am J Physiol Lung Cell Mol Physiol. 2012 January 15;302(2):L206-L215.
8.
Fig. 2.

Fig. 2. From: Human apolipoprotein E genotypes differentially modify house dust mite-induced airway disease in mice.

HDM-induced mucous cell metaplasia is reduced in humanized apoE ε3 mice. A and B: quantification of lung mRNA levels for Muc5AC and Clca3 by qRT-PCR presented as relative mRNA expression (n = 6 mice, *P < 0.05, huApoE + HDM vs. muApoE + HDM). C: mucous cell metaplasia presented as the percentage of airways containing PAS-positive cells (n = 10 mice, * P < 0.001, huApoE + HDM vs. muApoE + HDM ). On average, 40 ± 1 airways were inspected in each mouse. Results are representative of 2 independent experiments. PAS, periodic acid-Schiff.

Xianglan Yao, et al. Am J Physiol Lung Cell Mol Physiol. 2012 January 15;302(2):L206-L215.
9.
Fig. 1.

Fig. 1. From: Human apolipoprotein E genotypes differentially modify house dust mite-induced airway disease in mice.

Humanized apolipoprotein E (apoE) ε3 and ε4 mice are protected from house dust mite (HDM)-induced airway hyperreactivity. Airway hyperreactivity in wild-type C57BL/6 mice (murine apoE, muApoE) was compared with mice expressing human apoE2 (huApoE2) (A), apoE3 (huApoE3) (B), or apoE4 (huApoE4) (C) proteins, following daily nasal challenge with either saline (control) or HDM for 5 days per week for 5 wk. Airway resistance (cm H20/ml per s) was measured following nebulization of increasing doses of methacholine (n = 8–10 mice, *P < 0.001 at the 10 mg/ml dose of methacholine for huApoE + HDM vs. muApoE + HDM). Results are representative of 2 independent experiments.

Xianglan Yao, et al. Am J Physiol Lung Cell Mol Physiol. 2012 January 15;302(2):L206-L215.

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