ArticleInfection and immunity1999
Murine splenocytes induce severe gastritis and delayed-type hypersensitivity and suppress bacterial colonization in Helicobacter pylori-infected SCID mice.
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 101 citations in OpenAlex.
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- IL-17 Receptor Signaling through IL-17A or IL-17F Is Sufficient to Maintain Innate Response and Control ofImmunoHorizons · 2022Article
- The TNF-Alpha Inducing Protein is Associated With Gastric Inflammation and Hyperplasia in a Murine Model ofFrontiers in pharmacology · 2022Article
- WFDC2 Promotes Spasmolytic Polypeptide-Expressing Metaplasia Through the Up-Regulation of IL33 in Response to Injury.Gastroenterology · 2021Article
- Cytokine Profile of CCR6Sovremennye tekhnologii v meditsine · 2021Article
- Structure, metabolism and biological functions of steryl glycosides in mammals.The Biochemical journal · 2020Review
- T Cell Cytokines Impact Epithelial Cell Responses duringJournal of immunology (Baltimore, Md. : 1950) · 2020Review
- Regulation of Gastric Metaplasia, Dysplasia, and Neoplasia by Bone Morphogenetic Protein Signaling.Cellular and molecular gastroenterology and hepatology · 2017Review
- Early Molecular Events in Murine Gastric Epithelial Cells Mediated by Helicobacter pylori CagA.Helicobacter · 2016Article
- Anti-inflammatory activity of bone morphogenetic protein signaling pathways in stomachs of mice.Gastroenterology · 2014Article
- Complex T cell interactions contribute to Helicobacter pylori gastritis in mice.Infection and immunity · 2013Article
- Article
- Innate-like CD4 T cells selected by thymocytes suppress adaptive immune responses against bacterial infections.Open journal of immunology · 2012Article
- Lack of genetic influence on the innate inflammatory response to helicobacter infection of the gastric mucosa.Frontiers in immunology · 2012Article
- IL-23 Contributes to Control of Chronic Helicobacter Pylori Infection and the Development of T Helper Responses in a Mouse Model.Frontiers in immunology · 2012Article
- Helicobacter felis--associated gastric disease in microbiota-restricted mice.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2011Article
- Cationic amino acid transporter 2 enhances innate immunity during Helicobacter pylori infection.PloS one · 2011Article
- Fibroblastic colony-forming unit bone marrow cells delay progression to gastric dysplasia in a helicobacter model of gastric tumorigenesis.Stem cells (Dayton, Ohio) · 2009Article
- CD25+ T cells induce Helicobacter pylori-specific CD25- T-cell anergy but are not required to maintain persistent hyporesponsiveness.European journal of immunology · 2008Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The goal of this study was to evaluate the role of host immunity in gastritis and epithelial damage due to Helicobacter pylori. Splenocytes from H. pylori-infected and uninfected C57BL/6 mice were adoptively transferred to H. pylori-infected and uninfected severe combined immunodeficient (SCID) mice. Transfer was verified by flow cytometry, and all mice were evaluated for the presence of delayed-type hypersensitivity (DTH) by footpad inoculation with sterile H. pylori sonicate and for humoral immunity by enzyme-linked immunosorbent assay. The severity of gastritis and gastric epithelial damage was quantified histologically, epithelial proliferation was determined by proliferating cell nuclear antigen staining, and colonization was quantified by culture. C57BL/6 mice, but not nonrecipient SCID mice, developed moderate gastritis in response to H. pylori. In contrast, recipient SCID mice developed severe gastritis involving 50 to 100% of the gastric mucosa and strong DTH responses not present in C57BL/6 mice. DTH, but not serum anti-H. pylori immunoglobulin G, correlated with adoptive transfer, gastritis, and bacterial clearance. Severe gastritis, but not bacterial colonization, was associated with epithelial metaplasia, erosions, and an elevated labeling index. This study demonstrates that (i) adaptive immunity is essential for development of gastritis due to H. pylori in mice, (ii) T-cell-enriched lymphocytes in SCID mice induce DTH and gastritis, which is more severe than donor gastritis, and (iii) the host inflammatory response, not direct bacterial contact, causes epithelial damage. The greater severity of gastritis in recipient SCID mice than in donor C57BL/6 mice suggests that gastritis is due to specific T-cell subsets and/or the absence of regulatory cell subsets in the transferred splenocytes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.