Development of high-grade lymphoma in Helicobacter pylori -infected C57BL/6 miceNote

Wang, Xin; Wïllén, Roger; Andersson, Christina; Wadström, Torkel

doi:10.1034/j.1600-0463.2000.d01-89.x

Cited by 13 publications

(2 citation statements)

References 17 publications

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“…The results may also be remarkable in that a previous study observed no MALT lymphoma formation in WT mice infected with H. pylori Sydney strain 1 even after the 2-year follow-up period (42). Thus, Gal3-deficient mice may provide a useful model for the study of MALT lymphomagenesis by colonization with H. pylori Sydney strain 1 (43,44).…”

Section: Discussionmentioning

confidence: 55%

Galectin-3 Plays an Important Role in Innate Immunity to Gastric Infection by Helicobacter pylori

et al. 2016

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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.

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Section: Discussionmentioning

confidence: 55%

Galectin-3 Plays an Important Role in Innate Immunity to Gastric Infection by Helicobacter pylori

et al. 2016

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“…Epidemiological studies have further indicated that cagA-positive H. pylori is present in the gastric mucosa of most, if not all, patients with gastric mucosa-associated lymphoid tissue (MALT) lymphoma (Eck et al, 1997). Furthermore, mice infected with cagA-positive H. pylori develop severe gastritis and atrophic changes in their stomach (Sheu et al, 1999), followed by the development of MALT lymphoma (Wang et al, 2000). Together with the clinical observations that eradication of H. pylori by antibiotic therapy can lead to complete remission of MALT lymphoma (Wotherspoon et al, 1993), these observations provide evidence that cagA-positive H. pylori plays an important role in the development and/or maintenance of MALT lymphoma.…”

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confidence: 99%

Effects of Helicobacter pylori CagA protein on the growth and survival of B lymphocytes, the origin of MALT lymphoma

et al. 2003

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Neonatal Thymectomy Favors Helicobacter pylori–Promoted Gastric Mucosa-Associated Lymphoid Tissue Lymphoma Lesions in BALB/c Mice

Chrisment

Dubus

Chambonnier

et al. 2014

The American Journal of Pathology

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Neonatal thymectomy in BALB/c mice has been described as a model of gastric mucosa-associated lymphoid tissue (MALT) lymphoma (GML). By using this experimental system, we screened, for the first time to our knowledge, Helicobacter pylori GML-associated strains for their capacity to promote disease. A cohort of BALB/c mice underwent thymectomy at day 3 after birth (d3Tx). Successful thymic ablation was evaluated by the degree of lymphopenia in blood samples collected at 4 weeks of age. d3Tx and non-thymectomized controls were infected with either GML strains (B38 or B47) or control strains (SS1 or TN2GF4). Gastric samples collected at 6, 12, and 18 months after infection were studied for bacteria content, and submitted to histological, immunochemical, molecular, and immunological analyses. Severe gastric inflammation was only observed in d3Tx mice. In these animals, the gastric lamina propria was infiltrated with lymphoid cells organized in follicles composed of B cells with few infiltrating T cells. PCR of D/J IgH gene segments proved the monoclonality of infiltrating B cells, which strongly correlated with the presence of lymphoepithelial lesions. B-cell infiltrates were particularly prominent in mice infected with the B47-GML strain. No pathological changes were detected in noninfected d3Tx mice. We identified new H. pylori isolates adapted to the mouse stomach with high potential of GML development, which is only revealed in hosts rendered lymphopenic by neonatal thymic ablation.

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Development of high-grade lymphoma in Helicobacter pylori -infected C57BL/6 miceNote

Cited by 13 publications

References 17 publications

Galectin-3 Plays an Important Role in Innate Immunity to Gastric Infection by Helicobacter pylori

Galectin-3 Plays an Important Role in Innate Immunity to Gastric Infection by Helicobacter pylori

Effects of Helicobacter pylori CagA protein on the growth and survival of B lymphocytes, the origin of MALT lymphoma

Neonatal Thymectomy Favors Helicobacter pylori–Promoted Gastric Mucosa-Associated Lymphoid Tissue Lymphoma Lesions in BALB/c Mice

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