caa a22 4500 44579769X CHVBK 20180317145131.0 cr unu---uuuuu 170323e20111101xx s 000 0 eng 10.1007/s10620-011-1738-3 doi (NATIONALLICENCE)springer-10.1007/s10620-011-1738-3 Production of Ectopic Gastric Intrinsic Factor in Gastric Mucosa of Humans with Chronic Gastritis [Elektronische Daten] [J. Shao, R. Carmel, D. Alpers] Background: Ectopic expression of gastric intrinsic factor (IF) has been described in rodent models of chronic gastritis. Aims: The current study undertook to determine if ectopic IF was also present in chronic gastritis in humans and might identify the process of ectopic protein expression as part of the response to chronic injury. Methods: Archived biopsies from mid-body, angularis and prepylorus of 9 patients with and without chronic gastritis and food-cobalamin malabsorption were examined in a blinded fashion by immunocytochemistry as were biopsies from 5 normal subjects. Cells with ectopic IF were further examined with antibodies against pepsin or with Griffonia simplicifolia II (GSII) to identity cells in the mucous neck cell compartment. Results: Ectopic IF production in non-parietal cells was identified in cells that were H+,K+-ATPase-negative but IF-positive in 7 of the 9 patients (6/9 in the angularis and/or prepylorus biopsies and 1/9 only in the mid-body). These included 5 of the 6 H. pylori-infected patients and all 5 patients with severe food-cobalamin malabsorption. No normal control subjects demonstrated ectopic IF. The cells with ectopic IF were pepsinogen-positive peptic cells and were not GSII-positive. Expression was most extensive in patients and gastric regions with inflammation. In all but one sample, ectopic IF was observed near anatomical mucosal junctions, such as antral/body and prepylorus/duodenum junctions. Conclusions: These data in humans with and without gastritis are consistent with the hypothesis that local factors influence ectopic gastric IF expression, arising from either the anatomical location, the focal inflammation, or both. Springer Science+Business Media, LLC, 2011 Gastritis nationallicence Intrinsic factor nationallicence Parietal cells nationallicence Chief cells nationallicence Shao J. Department of Medicine, Washington University School of Medicine, St Louis, MO, USA aut Carmel R. Department of Medicine, New York Methodist Hospital, Brooklyn, NY, USA aut Alpers D. Department of Internal Medicine, Campus Box 8031, Washington University School of Medicine, 660 S Euclid Ave., 63130, St Louis, MO, USA aut Digestive Diseases and Sciences Springer US; http://www.springer-ny.com 56/11(2011-11-01), 3209-3219 0163-2116 56:11<3209 2011 56 10620 https://doi.org/10.1007/s10620-011-1738-3 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s10620-011-1738-3 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Shao J. Department of Medicine, Washington University School of Medicine, St Louis, MO, USA aut NATIONALLICENCE 700 1- Carmel R. Department of Medicine, New York Methodist Hospital, Brooklyn, NY, USA aut NATIONALLICENCE 700 1- Alpers D. Department of Internal Medicine, Campus Box 8031, Washington University School of Medicine, 660 S Euclid Ave., 63130, St Louis, MO, USA aut NATIONALLICENCE 773 0- Digestive Diseases and Sciences Springer US; http://www.springer-ny.com 56/11(2011-11-01), 3209-3219 0163-2116 56:11<3209 2011 56 10620 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer