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10.1128/IAI.01299-15 http://scihub22266oqcxt.onion/10.1128/IAI.01299-15 C4807496!4807496!26857579     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Infect+Immun 2016 ; 84 (4): 1184-93 Nephropedia Template TP {{tp|p=26857579|t=2016. Galectin-3 Plays an Important Role in Innate Immunity to Gastric Infection by Helicobacter pylori |pdf=|usr=}}{{26857579}} gab.com Text Galectin-3 Plays an Important Role in Innate Immunity to Gastric Infection by Helicobacter pylori JO: Infect Immun http://www.kidney.de/pget.php?&tw=1&pmid=26857579 #FOAvip We studied the role of galectin-3 (Gal3) in gastric infection by Helicobacter pylori. We first demonstrated that Gal3 was selectively expressed by gastric surface epithelial cells and abundantly secreted into the surface mucus layer. We next inoculated H. pylori Sydney strain 1 into wild-type (WT) and Gal3-deficient mice using a stomach tube. At 2 weeks postinoculation, the bacterial cells were mostly trapped within the surface mucus layer in WT mice. In sharp contrast, they infiltrated deep into the gastric glands in Gal3-deficient mice. Bacterial loads in the gastric tissues were also much higher in Gal3-deficient mice than in WT mice. At 6 months postinoculation, H. pylori had successfully colonized within the gastric glands of both WT and Gal3-deficient mice, although the bacterial loads were still higher in the latter. Furthermore, large lymphoid clusters mostly consisting of B cells were frequently observed in the gastric submucosa of Gal3-deficient mice. In vitro, peritoneal macrophages from Gal3-deficient mice were inefficient in killing engulfed H. pylori. Furthermore, recombinant Gal3 not only induced rapid aggregation of H. pylori but also exerted a potent bactericidal effect on H. pylori as revealed by propidium iodide uptake and a morphological shift from spiral to coccoid form. However, a minor fraction of bacterial cells, probably transient phase variants of Gal3-binding sugar moieties, escaped killing by Gal3. Collectively, our data demonstrate that Gal3 plays an important role in innate immunity to infection and colonization of H. pylori. Twit Text FOAVip Galectin-3 Plays an Important Role in Innate Immunity to Gastric Infection by Helicobacter pylori ????Infect Immun http://www.kidney.de/pget.php?&tw=1&pmid=26857579 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26857579 #FOAvip English Wikipedia <ref>{{Cite pmid|26857579}}</ref> Galectin-3 Plays an Important Role in Innate Immunity to Gastric Infection by Helicobacter pylori #MMPMID26857579 Park AM; Hagiwara S; Hsu DK; Liu FT; Yoshie O Infect Immun 2016[Apr]; 84 (4): 1184-93 PMID26857579show ga We studied the role of galectin-3 (Gal3) in gastric infection by Helicobacter pylori. We first demonstrated that Gal3 was selectively expressed by gastric surface epithelial cells and abundantly secreted into the surface mucus layer. We next inoculated H. pylori Sydney strain 1 into wild-type (WT) and Gal3-deficient mice using a stomach tube. At 2 weeks postinoculation, the bacterial cells were mostly trapped within the surface mucus layer in WT mice. In sharp contrast, they infiltrated deep into the gastric glands in Gal3-deficient mice. Bacterial loads in the gastric tissues were also much higher in Gal3-deficient mice than in WT mice. At 6 months postinoculation, H. pylori had successfully colonized within the gastric glands of both WT and Gal3-deficient mice, although the bacterial loads were still higher in the latter. Furthermore, large lymphoid clusters mostly consisting of B cells were frequently observed in the gastric submucosa of Gal3-deficient mice. In vitro, peritoneal macrophages from Gal3-deficient mice were inefficient in killing engulfed H. pylori. Furthermore, recombinant Gal3 not only induced rapid aggregation of H. pylori but also exerted a potent bactericidal effect on H. pylori as revealed by propidium iodide uptake and a morphological shift from spiral to coccoid form. However, a minor fraction of bacterial cells, probably transient phase variants of Gal3-binding sugar moieties, escaped killing by Gal3. Collectively, our data demonstrate that Gal3 plays an important role in innate immunity to infection and colonization of H. pylori. äGalectin-3 Plays an Important Role in Innate Immunity to Gastric Infec(epmc).pdf DeepDyve Pubget Overpricing