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Sustained Helicobacter pylori infection accelerates gastric dysplasia in a mouse model.
O'Brien, Valerie P; Koehne, Amanda L; Dubrulle, Julien; Rodriguez, Armando E; Leverich, Christina K; Kong, V Paul; Campbell, Jean S; Pierce, Robert H; Goldenring, James R; Choi, Eunyoung; Salama, Nina R.
Afiliación
  • O'Brien VP; Fred Hutchinson Cancer Research Center, Human Biology Division, Seattle, WA, USA.
  • Koehne AL; Fred Hutchinson Cancer Research Center, Comparative Medicine Shared Resource, Seattle, WA, USA.
  • Dubrulle J; Fred Hutchinson Cancer Research Center, Experimental Histopathology Shared Resource, Seattle, WA, USA.
  • Rodriguez AE; Fred Hutchinson Cancer Research Center, Genomics and Bioinformatics Shared Resource, Seattle, WA, USA.
  • Leverich CK; Fred Hutchinson Cancer Research Center, Human Biology Division, Seattle, WA, USA.
  • Kong VP; Fred Hutchinson Cancer Research Center, Human Biology Division, Seattle, WA, USA.
  • Campbell JS; Fred Hutchinson Cancer Research Center, Experimental Histopathology Shared Resource, Seattle, WA, USA.
  • Pierce RH; Fred Hutchinson Cancer Research Center, Program in Immunology, Seattle, WA, USA.
  • Goldenring JR; Fred Hutchinson Cancer Research Center, Program in Immunology, Seattle, WA, USA.
  • Choi E; Department of Surgery, Epithelial Biology Center, Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.
  • Salama NR; Nashville Veterans Affairs Medical Center, Nashville, TN, USA.
Life Sci Alliance ; 4(2)2021 02.
Article en En | MEDLINE | ID: mdl-33310760
More than 80% of gastric cancer is attributable to stomach infection with Helicobacter pylori (Hp). Gastric preneoplastic progression involves sequential tissue changes, including loss of parietal cells, metaplasia and dysplasia. In transgenic mice, active KRAS expression recapitulates these tissue changes in the absence of Hp infection. This model provides an experimental system to investigate additional roles of Hp in preneoplastic progression, beyond its known role in initiating inflammation. Tissue histology, gene expression, the immune cell repertoire, and metaplasia and dysplasia marker expression were assessed in KRAS+ mice +/-Hp infection. Hp+/KRAS+ mice had severe T-cell infiltration and altered macrophage polarization; a different trajectory of metaplasia; more dysplastic glands; and greater proliferation of metaplastic and dysplastic glands. Eradication of Hp with antibiotics, even after onset of metaplasia, prevented or reversed these tissue phenotypes. These results suggest that gastric preneoplastic progression differs between Hp+ and Hp- cases, and that sustained Hp infection can promote the later stages of gastric preneoplastic progression.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Gastropatías / Helicobacter pylori / Infecciones por Helicobacter Límite: Animals Idioma: En Revista: Life Sci Alliance Año: 2021 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Gastropatías / Helicobacter pylori / Infecciones por Helicobacter Límite: Animals Idioma: En Revista: Life Sci Alliance Año: 2021 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos