表紙・目次 『第15回CEReS国際シンポジウム「環境リモートセンシングのこれま での成果とさらなる挑戦」』 2009年12月15日～16日 於千葉大学

Held on 15-16 December, 2009, Chiba Universit

Cathepsin K transgenic mice (black bars) and wild-type mice (white bars) were administered either saline or bleomycin for 1, 2, 3, and 4 weeks

Subsequently, mice were euthanized and lungs were lavaged as described in Materials and Methods. Total BAL fluid cell numbers (A), alveolar macrophages (B), exudate macrophages (C), neutrophils (D) and lymphocytes (E) were ascertained from Pappenheim-stained cytospin preparations of BAL fluid. The data are shown as mean ± SD of at least n = 5 mice per group and time point. No statistical significances were noted between wild-type and Cathepsin K transgenic mice.<p><b>Copyright information:</b></p><p>Taken from "Overexpression of cathepsin K in mice decreases collagen deposition and lung resistance in response to bleomycin-induced pulmonary fibrosis"</p><p>http://respiratory-research.com/content/9/1/54</p><p>Respiratory Research 2008;9(1):54-54.</p><p>Published online 18 Jul 2008</p><p>PMCID:PMC2490691.</p><p></p

Overexpression of cathepsin K in mice decreases collagen deposition and lung resistance in response to bleomycin-induced pulmonary fibrosis-2

Nized and BAL cells (A, B), freshly isolated type II alveolar epithelial cells (A, C), lung homogenate (A, D), and concentrated BAL fluid supernatant (E) were prepared for analysis of cath K mRNA by real-time RT-PCR (A) and western blotting (B-E). (A), data are given as fold change in cathepsin K mRNA of bleomycin-challenged cath K tg mice compared to wild-type mice. (F) Gelatin zymography employing concentrated BAL fluid protein from mock- or bleomycin-treated wild-type mice and cath K tg mice. Data are shown as mean ± SD of n = 3 determinations. (B-F), data represent at least n = 3–5 independent analyses. * indicates < 0.05 versus bleomycin-treated wild-type mice at day 14 post-treatment.<p><b>Copyright information:</b></p><p>Taken from "Overexpression of cathepsin K in mice decreases collagen deposition and lung resistance in response to bleomycin-induced pulmonary fibrosis"</p><p>http://respiratory-research.com/content/9/1/54</p><p>Respiratory Research 2008;9(1):54-54.</p><p>Published online 18 Jul 2008</p><p>PMCID:PMC2490691.</p><p></p

Overexpression of cathepsin K in mice decreases collagen deposition and lung resistance in response to bleomycin-induced pulmonary fibrosis-1

Ks. Subsequently, mice were euthanized and lungs were processed for quantitative assessment of collagen content by hydroxyproline assay, as described in Materials and Methods. The data are shown as mean ± SD of at least n = 10 mice per group and time point. * indicates < 0.05 compared to wild-type mice. + indicates significant increase (p < 0.05) compared to mock-treated wild-type mice.<p><b>Copyright information:</b></p><p>Taken from "Overexpression of cathepsin K in mice decreases collagen deposition and lung resistance in response to bleomycin-induced pulmonary fibrosis"</p><p>http://respiratory-research.com/content/9/1/54</p><p>Respiratory Research 2008;9(1):54-54.</p><p>Published online 18 Jul 2008</p><p>PMCID:PMC2490691.</p><p></p

Cathepsin H function in production of lung surfactant proteins.

<p>(<b>A</b>) mRNA expression of surfactant proteins A1, B, and C measured by quantitative ‘real-time’ RT-PCR in lungs of <i>Ctsh^+/+</i> and <i>Ctsh</i>^−/− mice (n = 5 per group). (<b>B</b>) Detection of surfactant protein B (SP-B) in lung tissue lysates (<b>C</b>) Western blot detection of SP-B in broncho-alveolar lavage (BAL) of <i>Ctsh^+/+</i> and <i>Ctsh</i>^−/− mice of 2 genetic backgrounds (129P2/OlaHsd and C57BL/6N). The lysosomal membrane associated protein 2a (Lamp 2a) is present at the limiting membrane of lamellar bodies <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0026247#pone.0026247-Wasano1" target="_blank">[27]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0026247#pone.0026247-Albrecht1" target="_blank">[28]</a> and serves as loading control independent of the surfactant proteins. (<b>D</b>–<b>F</b>) Surface activity of BAL fluid measured by pulsating bubble surfactometry (n = 6–10).</p

Cathepsin expression and gross phenotype of Ctsh-deficient mice.

<p>(<b>A</b>) Western blots for Ctsh detection in lungs and liver of <i>Ctsh^+/+</i> and <i>Ctsh</i>^−/− mice. (<b>B</b>) Detection of “acidic” aminopeptidase activity at pH 6.0 in lungs, livers and kidneys of f <i>Ctsh^+/+</i> and <i>Ctsh</i>^−/− mice (n = 3). (<b>C</b>) Observed and expected genotype frequencies of litters from <i>Ctsh</i>^+/− x <i>Ctsh</i>^+/− matings. (<b>D</b>) Weight gain of female littermates from heterozygous matings (n = 5 per genotype). (<b>E</b>) mRNA expression of cathepsin C (Ctsc) and cathepsin E (Ctse) measured by quantitative ‘real-time’ RT-PCR in lungs of <i>Ctsh^+/+</i> and <i>Ctsh</i>^−/− mice (n = 5 per group). (<b>F</b>) Cathepsin C (Ctsc) and cathepsin E (Ctse) detected by Western blotting in <i>Ctsh^+/+</i> and <i>Ctsh</i>^−/− lung lysates.</p

Targeted disruption of the cathepsin H (Ctsh) gene.

<p>(<b>A</b>) Scheme for the targeted disruption of mouse Ctsh gene by homologous recombination. Exons are indicated by number. (<b>B</b>) Southern blot analysis of SacI-digested genomic DNA from mouse liver by the 5′ external probe denoted in panel A. Expected fragment sizes are 5.5 kb for wild-type and 6.8 kb for mutant <i>Ctsh</i> alleles. (<b>C</b>) Northern blots from liver and kidney samples of <i>Ctsh^+/+</i> and <i>Ctsh</i>^−/− mice. The Ctsh 5′ probe detects the genuine 1.6 kb mouse Ctsh transcript in the <i>Ctsh^+/+</i> samples. *Denotes an enlarged transcript in <i>Ctsh</i>^−/− consisting of Ctsh exons 1–5 plus lacZ reporter.</p

Effect of S100A9 deletion or reconstitution on lung antibacterial immunity in <i>S</i>. <i>pneumoniae</i>-infected bone-marrow chimeric mice.

(A) Endogenous S100A9 levels in BALF of chimeric mice on day 1 after pneumococcal challenge (n = 7–10 mice per group). (B,C) Bacterial loads in BAL fluids (B) and lung tissue (C) of S. pneumoniae-challenged chimeric mice on day 1 post-infection (n = 8–9 mice per group). (D) Zinc levels in lungs of S. pneumoniae-infected chimeric mice on day 1 post-infection, relative to controls (n = 8 mice per treatment group). Data are shown as means ± SD and are representative of two independently performed experiments. (E,F) Survival of chimeric mice infected with S. pneumoniae during an observation period of 10 days (n = 9–10 mice per group). The data represent two independent experiments. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001, ****p ≤ 0.0001 compared to chimeric controls, +p ≤ 0.05; ++p ≤ 0.01 compared to untreated controls (Kruskal-Wallis test, log-rank test).</p

Phagocytosis and burst induction in <i>S</i>. <i>pneumoniae</i>-infected alveolar macrophages and neutrophils of WT and S100A9 KO mice.

Cells were purified as described in Materials and Methods followed by infection with S. pneumoniae at a multiplicity of infection (MOI) of 25. (A,B) Phagocytosis capacity of resident AM (A) and bone marrow-derived neutrophils (BM-PMN) (B) at 30 or 60 minutes after infection of cells with S. pneumoniae. (C) Burst induction in purified BM-PMN of WT and S100A9 KO mice by S. pneumoniae (MOI 5). Data are representative of two independently performed experiments. (TIF)</p

Correlation between BAL fluid S100A9 and C-reactive protein in patients with bacterial or viral pneumonia.

(A) Positive correlation between BAL fluid S100A9 and C-reactive protein (CRP) in BAL fluids of patients with bacterial pneumonia (n = 17 patients). (B) Endogenous S100A9 protein in BAL fluids of patients with viral pneumonia was negatively correlated with C-reactive protein (n = 11 patients). (TIF)</p