C. S. Park and Sung-woo Park contributed equally as principal investigators of this research project.
Apolipoprotein A1 potentiates lipoxin A4 synthesis and recovery of allergen-induced disrupted tight junctions in the airway epithelium
Version of Record online: 29 JUL 2013
© 2013 John Wiley & Sons Ltd
Clinical & Experimental Allergy
Volume 43, Issue 8, pages 914–927, August 2013
How to Cite
Clinical & Experimental Allergy, 2013 (43) 914–927., , , , , , , , , , , .
- Issue online: 29 JUL 2013
- Version of Record online: 29 JUL 2013
- Accepted manuscript online: 4 MAY 2013 11:37AM EST
- Manuscript Accepted: 29 APR 2013
- Manuscript Revised: 21 APR 2013
- Manuscript Received: 19 OCT 2012
|cea12143-sup-0006-TableS1.pdf||application/PDF||83K||Table S1. Demographic characteristics of study subjects.|
|cea12143-sup-0001-FigS1.tif||image/tif||182K||Figure S1. Intranasal ApoA1 treatment inhibits lung dendritic cell accumulation in OVA-challenged mice. (a) On days 21–23, mice were instilled intratracheally with FITC-OVA. On days 24–25, ApoA1 was administered intranasally, and then the lungs were removed on day 26. Lungs were enzymatically digested and stained for the presence of FITC–MHCIIhigh–CD11Chigh–DCs, and subjected to flow cytometry. (b) In the same mice, the presence of FITC-migrating DCs in mediastinal lymph nodes was assessed. Results are representative of six mice per group. Experiments were repeated four times with similar results. Data are shown as means ± SEM. *P < 0.05.|
|cea12143-sup-0002-FigS2.tif||image/tif||4365K||Figure S2. Immunofluorescence of occludin (a) and Zo-1 (b) in primary BECs from asthmatics treated with ApoA1, mutant ApoA1, or co-treated with ApoA1 (1 μg/mL) and cinnamyl-3,4-dihydroxy-α-cyanocinnamate (CDC; 2 μM, 12/15-LOX inhibitor) was treated for 72 h. Scale bar = 20 μm.|
|cea12143-sup-0004-FigS3.tif||image/tif||472K||Figure S3. Intranasal co-administration of CDC and ApoA1 increased airway inflammation, airway hyperresponsiveness (AHR), and disruption of bronchial TJs in HDM-induced murine asthma. (a) Numbers of bronchoalveolar lavage (BAL) fluid cells in the four groups are shown as means ± SEM; **P < 0.01. (b) Fixed lung tissue specimens were sectioned and stained using H&E and periodic acid Schiff. (c) Airway resistance was measured following inhalation of increasing doses of methacholine. Each data point represents the mean ± SEM of six mice per group. *P < 0.05 HDM + ApoA1 + CDC vs. HDM + ApoA1. Data for Saline, HDM, and ApoA1 groups are from the same experiment represented in Fig. 1 and are included here for comparison with the data from the HDM + ApoA1 + CDC group (studied in the same experiments but not shown in Fig. 1).|
|cea12143-sup-0005-FigS4.tif||image/tif||140K||Figure S4. ApoA1 levels in BAL fluid from normal controls and subjects with asthma. ApoA1 concentration normalized to total protein as determined by ELISA. Data are presented as median values and interquartile ranges. **P < 0.01.|
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