Additional file 1: of Upregulation of interleukin-33 and thymic stromal lymphopoietin levels in the lungs of idiopathic pulmonary fibrosis

Supplemental data. (DOC 102 kb

Clinical characteristics of the study subjects.

<p>Values are mean ± SE. P-values are obtained using the <i>t</i>-test or the x²-test between AERD and ATA.</p><p>ATA: aspirin tolerant asthma, AERD : aspirin-exacerbated respiratory disease,</p><p>*P<0.05 compared with ATA.</p>†<p>D.f, D.p, Strawdust, Haydust, Cockroach mix, Chrysanthemum P, Aster P, Cat fur, Ragweed polle.</p

List of differentially expressed proteins identified by LC-MS.

<p>List of differentially expressed proteins identified by LC-MS.</p

Comparison of FABP1 expression in ATA and AERD patients.

<p>FABP1 abundance was measured in nasal polyp extract lysates of ATA (n = 3) and AERD (n = 3) patients using a mouse anti-human FABP1 monoclonal antibody. (A) Representative figure and (B) bar graph of the Western blot analysis of plasma from AERD and ATA samples.</p

Additional file 3: Figure S2. of Gene profile of fibroblasts identify relation of CCL8 with idiopathic pulmonary fibrosis

A heat map of 15,020 genes in IPF fibroblast and control fibroblast. A gradient scale ranging between green (down-regulated) and red (up-regulated) was indicated. The maximum value (red) of each gene was set to 3, the minimum value to −3, and the remaining values were linearly fitted in the range. (TIF 18692 kb

Additional file 2: Figure S1. of Gene profile of fibroblasts identify relation of CCL8 with idiopathic pulmonary fibrosis

Expression of epithelial, mesenchyal and myofibroblast markers of IPF fibroblasts and controls. Fibroblasts, obtained from lung biopsies of 14 IPF and normal lung sections of 10 subjects with localized lung cancer, was characterized using Western blot analysis for E-cadherin (epithelial marker), vimentin (mesenchymal cell marker) and ι-smooth muscle actin (myofibroblast marker). The expression levels were normalized to β-actin as an internal control protein. (TIF 8191 kb

Representative figure showing the immunohistochemical analysis of nasal polyps from ATA (n = 3) and AERD (n = 3) patients.

<p>A mouse anti-human FABP1 monoclonal antibody (1∶100 dilution), goat anti-human CD163 polyclonal antibodies (1∶100 dilution), goat anti-human MBP polyclonal antibodies (1∶100 dilution), and a mouse anti-human alpha smooth muscle actin monoclonal antibody (1∶50, clone 1A4, DAKO, Glostrup, Denmark) were used. Magnification: 400×.</p

Photographs of two-dimensional electrophoresis (2-DE) separation of nasal polyps proteins obtained from ATA (n = 8) and subjects with AERD (n = 5).

<p>(A) one ATA, and one patient with AERD. Nasal polyp proteins (1 mg) were focused on a pH 3–10 immobilized pH gradient strip and then separated by 7.5–20% gradient SDS-PAGE and visualized as described in the Methods. Protein spots identified by LC-MS (arrows) are labeled with numbers. Spot #2 is enlarged in small boxes. (B) The Y-axis of each graph represents the relative intensity of the spot (%). P-values represent the difference between the ATA and AERD samples.</p

Additional file 5: Figure S4. of Gene profile of fibroblasts identify relation of CCL8 with idiopathic pulmonary fibrosis

A blocking study using a recombinant CCL8 protein in Immunofluorescence staining of CCL8 protein. The mouse-anti human CCL8 antibody (1:100) were incubated with 10, 1, 0.1ng of a recombinant CCL8 (Origene, Rockville, MD, USA) for 2 h at room temperature, then the mixtures were incubated for overnight with the tissue sections of IPF lung tissues at 4 °C. The 2nd Ab (rabbit anti-mouse-PE 1:2000) was incubated for 2 h and Confocal laser scanning was performed using a microscope. As shown in the pictures, intensity of CCL8 staining was decreased as the concentration of recombinant CCL8 protein increased. (TIF 8134 kb

A Genome-Wide Association Study of Total Serum and Mite-Specific IgEs in Asthma Patients

<div><p>Immunoglobulin E (IgE) is one of the central players in asthma and allergic diseases. Although the serum IgE level, a useful endophenotype, is generally increased in patients with asthma, genetic factors influencing IgE regulation in asthma are still not fully understood. To identify the genetic variations associated with total serum and mite-specific IgEs in asthmatics, a genome-wide association study (GWAS) of 657,366 single nucleotide polymorphisms (SNPs) was performed in 877 Korean asthmatics. This study found that several new genes might be associated with total IgE in asthmatics, such as <i>CRIM1</i> (rs848512, <i>P</i> = 1.18×10⁻⁶; rs711254, <i>P</i> = 6.73×10⁻⁶), <i>ZNF71</i> (rs10404342, <i>P</i> = 7.60×10⁻⁶), <i>TLN1</i> (rs4879926, <i>P</i> = 7.74×10⁻⁶), and <i>SYNPO2</i> (rs1472066, <i>P</i> = 8.36×10⁻⁶; rs1038770, <i>P</i> = 8.66×10⁻⁶). Regarding the association of specific IgE to house dust mites, it was observed that intergenic SNPs nearby to <i>OPRK1</i> and <i>LOC730217</i> might be associated with <i>Dermatophagoides pteronyssinus</i> (D.p.) and <i>Dermatophagoides farinae</i> (D.f.) in asthmatics, respectively. In further pathway analysis, the phosphatidylinositol signaling system and adherens junction pathways were estimated to play a role in the regulation of total IgE levels in asthma. Although functional evaluations and replications of these results in other populations are needed, this GWAS of serum IgE in asthmatics could facilitate improved understanding of the role of the newly identified genetic variants in asthma and its related phenotypes.</p></div