ArticleInnate immunity2018
Helicobacter pylori controls NLRP3 expression by regulating hsa-miR-223-3p and IL-10 in cultured and primary human immune cells.
Article in Innate immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 48 citations in OpenAlex.
- Gastrointestinal inflammation and cancer: viral and bacterial interplay.Gut microbes · 2025Review
- Role of NLRP3 Inflammasomes in Disorders of Children's Digestive Systems: A Narrative Review.Pediatric reports · 2025Review
- H. pylori infection downregulates the expression and release of miR- 223 in neutrophils.International microbiology : the official journal of the Spanish Society for Microbiology · 2025Article
- Investigation of the mechanism by which miR-223-3p inhibits reflux esophagitis through targeting the NLRP3 inflammasome.BMC gastroenterology · 2025Article
- Mechanism and role of H. pylori CagA-induced NLRP3 inflammasome in gastric cancer immune cell infiltration.Scientific reports · 2025Article
- Molecular insights into NLRP3 inflammasome and miRNA modulation in oral cancer.Frontiers in pharmacology · 2025Review
- Inflammatory factors collaboratively linkFrontiers in immunology · 2025Review
- Review
- The current landscape of microRNAs (miRNAs) in bacterial pneumonia: opportunities and challenges.Cellular & molecular biology letters · 2022Review
- Old and New Aspects ofChildren (Basel, Switzerland) · 2022Review
- H. pylori CagA activates the NLRP3 inflammasome to promote gastric cancer cell migration and invasion.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Review
- The role of non-coding RNA in the diagnosis and treatment ofFrontiers in medicine · 2022Review
- NLRP3 inflammasome in digestive diseases: From mechanism to therapy.Frontiers in immunology · 2022Review
- MicroRNA‑502‑3p promotesMolecular medicine reports · 2021Article
- MiR-223-3p inhibits inflammation and pyroptosis in monosodium urate-induced rats and fibroblast-like synoviocytes by targeting NLRP3.Clinical and experimental immunology · 2021Article
- Apoptosis inhibitor of macrophage (AIM) contributes to IL-10-induced anti-inflammatory response through inhibition of inflammasome activation.Cell death & disease · 2021Article
- Non-Coding RNAs: Master Regulators of Inflammasomes in Inflammatory Diseases.Journal of inflammation research · 2021Review
- Article
- Immune Response inGastroenterology research and practice · 2020Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammasome-mediated production of mature IL-1β and IL-18 cytokines represents an important innate immune response against infecting pathogens. Helicobacter pylori, one of the most successful and persistent human pathogens, induces severe inflammation leading to gastritis and more serious gastric diseases. H. pylori modulates different immune responses for its survival and inflammasome signaling is manipulated by the cag pathogenicity island ( cagPAI), urease and VacA cytotoxin. Here we report that H. pylori regulates NLRP3 expression, an inflammasome forming regulator, in infected THP-1 monocytes. This response was independent of the major H. pylori pathogenicity-associated factors CagA, VacA, Cgt, FlaA and cagPAI. Two NLRP3 expression controlling factors, the NLRP3 mRNA targeting microRNA hsa-miR-223-3p and cytokine IL-10, were found to work in tandem for its regulation. H. pylori infection also induced copious amount of pro-IL-1β in THP-1 monocytes/macrophages but secreted a very low amount of mature IL-1β. Moreover, secreted IL-10 correlated with the down-regulation of nigericin-induced NLRP3 inflammasome activation of LPS-primed THP-1 monocytes and human PBMCs from volunteers. However, H. pylori-treated PBMCs secreted significantly more mature IL-1β throughout the infection period, which suggests a different mode of activation. Taken together, this study demonstrates targeting of inflammasome-forming NLRP3, an important innate immunity component, and crucial manipulation of pro- and anti-inflammatory cytokines in H. pylori infection.
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Registered trials
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