Helicobacter pylori Modulates Lymphoepithelial Cell Interactions Leading to Epithelial Cell Damage through Fas/Fas Ligand Interactions
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| Published in | Infection and Immunity Vol. 68; no. 7; pp. 4303 - 4311 |
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01.07.2000
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| AbstractList | Helicobacter pylori causes a common chronic infection of humans that leads to epithelial cell damage. Studies have shown that apoptosis of the gastric epithelium is increased during infection and this response is associated with an expansion of gastric T-helper type 1 (Th1) cells. We report that gastric T cells contribute to apoptosis of the epithelium by a Fas/Fas ligand (FasL) interaction. Fas receptor expression was detected on freshly isolated gastric epithelial cells by flow cytometry and immunohistochemistry, and this level of expression was increased during infection with H. pylori. The expression of Fas receptor on three gastric epithelial cell lines was increased by H. pylori, either alone or in combination with gamma interferon or tumor necrosis factor alpha. The role of Fas in apoptosis of gastric epithelial cell lines was evidenced by DNA fragmentation after crosslinking of Fas with specific antibodies. FasL expression was detected by immunohistochemistry on mononuclear cells in gastric biopsy specimens of infected but not uninfected subjects. Gastric T-cell lines were also shown to express FasL, as evidenced by reverse transcription-PCR and killing of target cells expressing Fas receptor. Moreover, these T-cell lines were capable of killing cultured gastric epithelial target cells and antibodies that block the interaction between Fas receptor and FasL inhibited this cytotoxic activity. These observations demonstrate that local Th1 cells may contribute to the pathogenesis of gastric disease during H. pylori infection by increasing the expression of Fas on gastric epithelial cells and inducing apoptosis through Fas/FasL interactions. Helicobacter pylori causes a common chronic infection of humans that leads to epithelial cell damage. Studies have shown that apoptosis of the gastric epithelium is increased during infection and this response is associated with an expansion of gastric T-helper type 1 (Th1) cells. We report that gastric T cells contribute to apoptosis of the epithelium by a Fas/Fas ligand (FasL) interaction. Fas receptor expression was detected on freshly isolated gastric epithelial cells by flow cytometry and immunohistochemistry, and this level of expression was increased during infection with H. pylori. The expression of Fas receptor on three gastric epithelial cell lines was increased by H. pylori, either alone or in combination with gamma interferon or tumor necrosis factor alpha. The role of Fas in apoptosis of gastric epithelial cell lines was evidenced by DNA fragmentation after cross-linking of Fas with specific antibodies. FasL expression was detected by immunohistochemistry on mononuclear cells in gastric biopsy specimens of infected but not uninfected subjects. Gastric T-cell lines were also shown to express FasL, as evidenced by reverse transcription-PCR and killing of target cells expressing Fas receptor. Moreover, these T-cell lines were capable of killing cultured gastric epithelial target cells and antibodies that block the interaction between Fas receptor and FasL inhibited this cytotoxic activity. These observations demonstrate that local Th1 cells may contribute to the pathogenesis of gastric disease during H. pylori infection by increasing the expression of Fas on gastric epithelial cells and inducing apoptosis through Fas/FasL interactions. Helicobacter pylori causes a common chronic infection of humans that leads to epithelial cell damage. Studies have shown that apoptosis of the gastric epithelium is increased during infection and this response is associated with an expansion of gastric T-helper type 1 (Th1) cells. We report that gastric T cells contribute to apoptosis of the epithelium by a Fas/Fas ligand (FasL) interaction. Fas receptor expression was detected on freshly isolated gastric epithelial cells by flow cytometry and immunohistochemistry, and this level of expression was increased during infection with H. pylori. The expression of Fas receptor on three gastric epithelial cell lines was increased by H. pylori, either alone or in combination with gamma interferon or tumor necrosis factor alpha. The role of Fas in apoptosis of gastric epithelial cell lines was evidenced by DNA fragmentation after cross-linking of Fas with specific antibodies. FasL expression was detected by immunohistochemistry on mononuclear cells in gastric biopsy specimens of infected but not uninfected subjects. Gastric T-cell lines were also shown to express FasL, as evidenced by reverse transcription-PCR and killing of target cells expressing Fas receptor. Moreover, these T-cell lines were capable of killing cultured gastric epithelial target cells and antibodies that block the interaction between Fas receptor and FasL inhibited this cytotoxic activity. These observations demonstrate that local Th1 cells may contribute to the pathogenesis of gastric disease during H. pylori infection by increasing the expression of Fas on gastric epithelial cells and inducing apoptosis through Fas/FasL interactions.Helicobacter pylori causes a common chronic infection of humans that leads to epithelial cell damage. Studies have shown that apoptosis of the gastric epithelium is increased during infection and this response is associated with an expansion of gastric T-helper type 1 (Th1) cells. We report that gastric T cells contribute to apoptosis of the epithelium by a Fas/Fas ligand (FasL) interaction. Fas receptor expression was detected on freshly isolated gastric epithelial cells by flow cytometry and immunohistochemistry, and this level of expression was increased during infection with H. pylori. The expression of Fas receptor on three gastric epithelial cell lines was increased by H. pylori, either alone or in combination with gamma interferon or tumor necrosis factor alpha. The role of Fas in apoptosis of gastric epithelial cell lines was evidenced by DNA fragmentation after cross-linking of Fas with specific antibodies. FasL expression was detected by immunohistochemistry on mononuclear cells in gastric biopsy specimens of infected but not uninfected subjects. Gastric T-cell lines were also shown to express FasL, as evidenced by reverse transcription-PCR and killing of target cells expressing Fas receptor. Moreover, these T-cell lines were capable of killing cultured gastric epithelial target cells and antibodies that block the interaction between Fas receptor and FasL inhibited this cytotoxic activity. These observations demonstrate that local Th1 cells may contribute to the pathogenesis of gastric disease during H. pylori infection by increasing the expression of Fas on gastric epithelial cells and inducing apoptosis through Fas/FasL interactions. Classifications Services IAI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue IAI About IAI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy Connect to IAI IAI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0019-9567 Online ISSN: 1098-5522 Copyright © 2014 by the American Society for Microbiology. For an alternate route to IAI .asm.org, visit: IAI Helicobacter pylori causes a common chronic infection of humans that leads to epithelial cell damage. Studies have shown that apoptosis of the gastric epithelium is increased during infection and this response is associated with an expansion of gastric T-helper type 1 (Th1) cells. We report that gastric T cells contribute to apoptosis of the epithelium by a Fas/Fas ligand (FasL) interaction. Fas receptor expression was detected on freshly isolated gastric epithelial cells by flow cytometry and immunohistochemistry, and this level of expression was increased during infection with H. pylori . The expression of Fas receptor on three gastric epithelial cell lines was increased by H. pylori , either alone or in combination with gamma interferon or tumor necrosis factor alpha. The role of Fas in apoptosis of gastric epithelial cell lines was evidenced by DNA fragmentation after cross-linking of Fas with specific antibodies. FasL expression was detected by immunohistochemistry on mononuclear cells in gastric biopsy specimens of infected but not uninfected subjects. Gastric T-cell lines were also shown to express FasL, as evidenced by reverse transcription-PCR and killing of target cells expressing Fas receptor. Moreover, these T-cell lines were capable of killing cultured gastric epithelial target cells and antibodies that block the interaction between Fas receptor and FasL inhibited this cytotoxic activity. These observations demonstrate that local Th1 cells may contribute to the pathogenesis of gastric disease during H. pylori infection by increasing the expression of Fas on gastric epithelial cells and inducing apoptosis through Fas/FasL interactions. |
| Author | Michael Bennett Joe O'Connoll Peter B. Ernst Victor E. Reyes Catharina Lindholm Fergus Shanahan Edward G. Brooks Jide Wang Xuejun Fan |
| AuthorAffiliation | Departments of Pediatrics 1 and Microbiology & Immunology 4 and Sealy Center for Molecular Sciences, 5 University of Texas Medical Branch, Galveston, Texas, 77555-0366; Department of Medical Microbiology and Immunology, University of Göteborg, Göteborg, Sweden 2 ; and Department of Medicine, National University of Ireland, Cork, Ireland 3 |
| AuthorAffiliation_xml | – name: Departments of Pediatrics 1 and Microbiology & Immunology 4 and Sealy Center for Molecular Sciences, 5 University of Texas Medical Branch, Galveston, Texas, 77555-0366; Department of Medical Microbiology and Immunology, University of Göteborg, Göteborg, Sweden 2 ; and Department of Medicine, National University of Ireland, Cork, Ireland 3 |
| Author_xml | – sequence: 1 givenname: J surname: Wang fullname: Wang, J organization: Departments of Pediatrics, University of Texas Medical Branch, Galveston, Texas 77555-0366, USA – sequence: 2 givenname: X surname: Fan fullname: Fan, X – sequence: 3 givenname: C surname: Lindholm fullname: Lindholm, C – sequence: 4 givenname: M surname: Bennett fullname: Bennett, M – sequence: 5 givenname: J surname: O'Connoll fullname: O'Connoll, J – sequence: 6 givenname: F surname: Shanahan fullname: Shanahan, F – sequence: 7 givenname: E G surname: Brooks fullname: Brooks, E G – sequence: 8 givenname: V E surname: Reyes fullname: Reyes, V E – sequence: 9 givenname: P B surname: Ernst fullname: Ernst, P B |
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| Keywords | Stomach Spirillales Digestive system Pathogenesis Spirillaceae Helper cell Molecular interaction Host agent relation Epithelium In vitro Mechanism Pathogenicity Helicobacter pylori Cell death T-Lymphocyte Bacteria Apoptosis |
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| Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 Corresponding author. Mailing address: Children's Hospital Rm 2.300, UTMB, 301 University Blvd., Galveston, TX 77555-0366. Phone: (409) 772-1750. Fax: (409) 772-1761. E-mail: Pernst@utmb.edu. |
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Reddit... Helicobacter pylori causes a common chronic infection of humans that leads to epithelial cell damage. Studies have shown that apoptosis of the gastric... Helicobacter pylori causes a common chronic infection of humans that leads to epithelial cell damage. Studies have shown that apoptosis of the gastric... |
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| StartPage | 4303 |
| SubjectTerms | Adult Apoptosis Bacteriology Base Sequence Biological and medical sciences Cell Line Cytokines - biosynthesis DNA Primers - genetics Epithelial Cells - immunology Epithelial Cells - pathology Fas antigen Fas Ligand Protein fas Receptor - metabolism FasL protein Fundamental and applied biological sciences. Psychology Gastric Mucosa - immunology Gastric Mucosa - pathology Gastritis - genetics Gastritis - immunology Gastritis - pathology Helicobacter Infections - genetics Helicobacter Infections - immunology Helicobacter Infections - pathology Helicobacter pylori Helicobacter pylori - pathogenicity Host Response and Inflammation Humans Lymphoid Tissue - immunology Lymphoid Tissue - pathology Membrane Glycoproteins - genetics Membrane Glycoproteins - metabolism Microbiology Middle Aged Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains Th1 Cells - immunology Th1 Cells - pathology |
| Title | Helicobacter pylori Modulates Lymphoepithelial Cell Interactions Leading to Epithelial Cell Damage through Fas/Fas Ligand Interactions |
| URI | http://iai.asm.org/content/68/7/4303.abstract https://www.ncbi.nlm.nih.gov/pubmed/10858249 https://www.proquest.com/docview/17611319 https://www.proquest.com/docview/71189904 https://pubmed.ncbi.nlm.nih.gov/PMC101751 |
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