ArticleHelicobacter2011
Effects of myeloid differentiation primary response gene 88 (MyD88) activation on Helicobacter infection in vivo and induction of a Th17 response.
Article in Helicobacter, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Genetic polymorphisms and tissue expression of interleukin-22 associated with risk and therapeutic response of gastric mucosa-associated lymphoid tissue lymphoma.Blood cancer journal · 2014Trial
- [Molecular mechanisms of chronic gastric mucosal inflammation induced byZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Review
- TRIF-IFN-I pathway iniScience · 2024Article
- The TLR/MyD88 signalling cascade in inflammation and gastric cancer: the immune regulatory network of Helicobacter pylori.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Early detection of tumor cells in bone marrow and peripheral blood in a fast‑progressing gastric cancer model.International journal of oncology · 2021Article
- Microbiome Signatures in a Fast- and Slow-Progressing Gastric Cancer Murine Model and Their Contribution to Gastric Carcinogenesis.Microorganisms · 2021Article
- Increased LIGHT expression and activation of non-canonical NF-κB are observed in gastric lesions of MyD88-deficient mice upon Helicobacter felis infection.Scientific reports · 2019Article
- Article
- IL-22-induced antimicrobial peptides are key determinants of mucosal vaccine-induced protection against H. pylori in mice.Mucosal immunology · 2017Article
- In vivo treatment of Helicobacter pylori infection with liposomal linolenic acid reduces colonization and ameliorates inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Deficiency of the myeloid differentiation primary response molecule MyD88 leads to an early and rapid development of Helicobacter-induced gastric malignancy.Infection and immunity · 2014Article
- IL-22 negatively regulates Helicobacter pylori-induced CCL20 expression in gastric epithelial cells.PloS one · 2014Article
- Gli1 deletion prevents Helicobacter-induced gastric metaplasia and expansion of myeloid cell subsets.PloS one · 2013Article
- Inflammation, immunity, and vaccines for Helicobacter pylori infection.Helicobacter · 2012Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundHelicobacter pylori is a spiral-shaped Gram-negative microaerophilic bacterium associated with a number of gastrointestinal disorders, including gastritis, peptic ulcers, and gastric cancer. Several studies have implicated a Th17 response as a key to protective immunity against Helicobacter. MATERIALS AND
methodsWild type (WT) and MyD88-deficient (MyD88(-/-)) mice in the C57BL/6 background were infected with H. felis for 6 and 25 weeks and colonization density and host response evaluated. Real-time PCR was used to determine the expression of cytokines and antimicrobial peptides in the gastric tissue of mice.
resultsmRNA expression levels of the Th17 cytokines interleukin-17A (IL-17A) and IL-22 were markedly up-regulated in WT compared with MyD88(-/-) mice both at 6 and at 25 weeks in response to infection with H. felis, indicating that induction of Th17 responses depends on MyD88 signaling. Furthermore, reduction in the expression of Th17-dependent intestinal antimicrobial peptide lipocalin-2 was linked with increased bacterial burden in the absence of MyD88 signaling.
conclusionWe provide evidence showing that MyD88-dependent signaling is required for the host to induce a Th17 response for the control of Helicobacter infection.
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Registered trials
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.