ArticlePloS one2009
A commensal Helicobacter sp. of the rodent intestinal flora activates TLR2 and NOD1 responses in epithelial cells.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Nervonic Acid Prevents HFD-Induced Metabolic Dysfunction and Is Associated with Gut Microbiota Remodeling.Metabolites · 2026Article
- Avian Aquatic Reservoirs and Zoonotic Potential of Helicobacter spp. in Wetlands from the Southern Caribbean Sea.Current microbiology · 2026Article
- Incorporation of polylactic acid microplastics into the carbon cycle as a carbon source to remodel the endogenous metabolism of the gut.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Investigation of the nutritional and functional roles of a microencapsulated blend of botanicals on intestinal health and growth of nursery pigs challenged with F18+Escherichia coli.Journal of animal science · 2025Article
- Mouse Models Of Helicobacter Infection And Gastric Pathologies.Journal of visualized experiments : JoVE · 2018Article
- NKT cells contribute to basal IL-4 production but are not required to induce experimental asthma.PloS one · 2017Article
- Pattern-recognition receptors and gastric cancer.Frontiers in immunology · 2014Review
- Therapeutic targeting of NOD1 receptors.British journal of pharmacology · 2013Review
- Helicobacter bilis gamma-glutamyltranspeptidase enhances inflammatory stress response via oxidative stress in colon epithelial cells.PloS one · 2013Article
- H. pylori exploits and manipulates innate and adaptive immune cell signaling pathways to establish persistent infection.Cell communication and signaling : CCS · 2011Article
- Coinfection with Enterohepatic Helicobacter species can ameliorate or promote Helicobacter pylori-induced gastric pathology in C57BL/6 mice.Infection and immunity · 2011Article
- Article
- Helicobacter hepaticus infection in mice: models for understanding lower bowel inflammation and cancer.Mucosal immunology · 2011Review
- Hemorrhage-induced intestinal damage is complement-independent in Helicobacter hepaticus-infected mice.Shock (Augusta, Ga.) · 2010Article
- The bacterial signal indole increases epithelial-cell tight-junction resistance and attenuates indicators of inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Quantitative analysis of the immune response upon Salmonella typhimurium infection along the porcine intestinal gut.Veterinary researchArticle
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
Abstract
Helicobacter spp. represent a proportionately small but significant component of the normal intestinal microflora of animal hosts. Several of these intestinal Helicobacter spp. are known to induce colitis in mouse models, yet the mechanisms by which these bacteria induce intestinal inflammation are poorly understood. To address this question, we performed in vitro co-culture experiments with mouse and human epithelial cell lines stimulated with a selection of Helicobacter spp., including known pathogenic species as well as ones for which the pathogenic potential is less clear. Strikingly, a member of the normal microflora of rodents, Helicobacter muridarum, was found to be a particularly strong inducer of CXC chemokine (Cxcl1/KC, Cxcl2/MIP-2) responses in a murine intestinal epithelial cell line. Time-course studies revealed a biphasic pattern of chemokine responses in these cells, with H. muridarum lipopolysaccharide (LPS) mediating early (24-48 h) responses and live bacteria seeming to provoke later (48-72 h) responses. H. muridarum LPS per se was shown to induce CXC chemokine production in HEK293 cells stably expressing Toll-like receptor 2 (TLR2), but not in those expressing TLR4. In contrast, live H. muridarum bacteria were able to induce NF-kappaB reporter activity and CXC chemokine responses in TLR2-deficient HEK293 and in AGS epithelial cells. These responses were attenuated by transient transfection with a dominant negative construct to NOD1, and by stable expression of NOD1 siRNA, respectively. Thus, the data suggest that both TLR2 and NOD1 may be involved in innate immune sensing of H. muridarum by epithelial cells. This work identifies H. muridarum as a commensal bacterium with pathogenic potential and underscores the potential roles of ill-defined members of the normal flora in the initiation of inflammation in animal hosts. We suggest that H. muridarum may act as a confounding factor in colitis model studies in rodents.
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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.