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Additional file 2. Supplementary Tables 1–4: Table 1. Cox proportional hazard analysis of overall survival. Table 2. Cox proportional hazard analysis of acute exacerbations. Table 3. Characteristics of the new clusters derived from Cluster II. Table 4. Diagnosis of IIPs in the new clusters derived from Cluster II.

Additional file 1: Table S1. Reasons for IIPs being unclassified in MDD.

Additional file 1. Supplementary Figures 1–3: Figure 1. Dendrogram of patients with IIPs using cluster analysis. Figure 2. Overall survival in the new clusters derived from Cluster II. Figure 3. Cumulative incidence of acute exacerbations in the new clusters derived from Cluster II.

Additional file 3: Fig. S1. Correlation between BAL lymphocytes and interstitial cell infiltration on histopathological examination in a subgroup of patients without anti-inflammatory drugs.

Additional file 4: Fig. S2. Prognostic impact of BAL lymphocytosis on patients treated with anti-inflammatory drugs at each cut-off value

Additional file 2: Table S2. Environmental exposures, symptoms suggestive of CTD, and serologic markers associated with CTD

Additional file 5: Fig. S3. CART analysis for predicting prognosis.

Additional file 5: Fig. S1. IAV RNA levels in organ culture of murine tracheal tissues. Fig. S2. Inactivation of IAV by UV irradiation. Fig. S3. IAV RNA levels in tracheal tissues of WT and TLR3-KO mice. Fig. S4. Changes of CBF by ATP stimulation.

Additional file 1 Figure S1. Quantification of CD248-positive fibroblast-like cells and ITGA8-positive fibroblast-like cells in collagen fiber-rich connective tissue and elastic fiber-rich connective tissue in IPF lungs. Figure S2. Osteoblast differentiation in mouse fibroblast subtypes. Figure S3. Cell cycle of mouse fibroblast subtypes were analyzed using 5-ethynyl-2′-deoxyuridine (EdU). Figure S4. Expression levels of Sca-1 and Itga8 during mouse fibroblast culture. Figure S5. Multiple immunofluorescence (IF) images of pulmonary artery wall (media and adventitia) of normal human lung. Figure S6. Multiple IF images of visceral pleura of normal human lung. Figure S7. Localization of CD248highITGA8low fibroblast-like cells and CD248lowITGA8high fibroblast-like cells in other major human organs. Figure S8. Graphical description of the digital image analysis using the Color Deconvolution ImageJ plugin. Table S1. Details of the antibodies used in this study. Table S2. Microarray analysis results of pulmonary single cells and three immunophenotypically distinct mouse fibroblast types. Table S3. Specific markers associated with Sca-1low mouse fibroblast (C-type fibroblast)-specific genes. Table S4. Specific markers associated with Sca-1high mouse fibroblast (A- and B-type fibroblast)-specific genes. Table S5. Primers used for quantitative PCR used in this study. Table S6. The demographic and clinical data of 10 patients with histologically confirmed IPF.

Figure S1. Purity of magnetically sorted mouse lung CD45−CD31+ cells. The purity was confirmed using flow cytometry with antibodies to CD31 and CD45. Representative example of dot plots obtained from magnetically sorted mouse lung CD45−CD31+ cells. Figures indicate percentages of cells expressing CD45 and CD31. The purity was > 90% in the three experiments. (PDF 124 kb)

Table S1. Primers used for quantitative real-time PCR. (DOCX 21 kb)

Figure S2. TGF-β1 concentrations in BAL fluid after administration of bleomycin. TGF-β1 concentrations in BAL fluid were gradually increased, with a significant increase on day 21 after bleomycin treatment (p = 0.0025 and p = 0.0235, compared with saline-treated mice and bleomycin-treated mice on day 7, respectively). (PDF 21 kb)

Baseline characteristics of all subjects included in this study. Table S2. Comparison of baseline characteristics between patients with higher and lower values of serum soluble CD163 (cutoff 800Â ng/mL). (DOCX 45 kb)

Intracellular invasion of NTHi in the presence of increasing dose of heparin. BEAS-2B cells were pretreated with several concentrations of heparin. These cells were infected for 2Â hours with one of the two NTHi strains ((A) ATCC 19418 or (B) HUSM 0481). After killing extracellular bacteria with gentamicin, the BEAS-2B cells were lysed. The number of colonies was counted and the percentages of CFU after gentamicin treatment of cells per input CFU were shown. Error bars represent SEM in three independent experiments that gave similar results. *pâ

Expression of vitronectin in BEAS-2B cells. BEAS-2B cells were stained with mouse anti-human vitronectin-antibody (primary antibody) and then with goat anti-mouse IgG antibody (secondary antibody, yellow). Nuclei were stained with Hoechst (blue). Representative fluorescent micrographs at 1,000Ă magnification are shown. (A) BEAS-2B cells were stained with the secondary antibody without the primary antibody. (B) Uninfected BEAS-2B cells. (C) BEAS-2B cells infected with NTHi. White bars represent 10Â Îźm. (PPTX 4302 kb)

Intracellular invasion of NTHi in the presence of increasing dose of heparin. BEAS-2B cells were pretreated with several concentrations of heparin. These cells were infected for 2Â hours with one of the two NTHi strains ((A) ATCC 19418 or (B) HUSM 0481). After killing extracellular bacteria with gentamicin, the BEAS-2B cells were lysed. The number of colonies was counted and the percentages of CFU after gentamicin treatment of cells per input CFU were shown. Error bars represent SEM in three independent experiments that gave similar results. *pâ