ArticleInflammatory bowel diseases2010
MDP-NOD2 stimulation induces HNP-1 secretion, which contributes to NOD2 antibacterial function.
Article in Inflammatory bowel diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
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- Targeting Intestinal Permeability for Graft-versus-Host Disease Treatment: A Therapeutic Perspective with Defibrotide.Journal of experimental pharmacology · 2025Article
- Peptidoglycan-induced modulation of metabolic and inflammatory responses.Immunometabolism (Cobham, Surrey) · 2023Review
- The Role of Antimicrobial Peptides in Preterm Birth.International journal of molecular sciences · 2021Review
- GRIM-19 Ameliorates Multiple Sclerosis in a Mouse Model of Experimental Autoimmune Encephalomyelitis with Reciprocal Regulation of IFNγ/Th1 and IL-17A/Th17 Cells.Immune network · 2020Article
- An Update Review on the Paneth Cell as Key to Ileal Crohn's Disease.Frontiers in immunology · 2020Review
- NOD2 Expression in Intestinal Epithelial Cells Protects Toward the Development of Inflammation and Associated Carcinogenesis.Cellular and molecular gastroenterology and hepatology · 2019Review
- Caspase recruitment domain (CARD) family (CARD9, CARD10, CARD11, CARD14 and CARD15) are increased during active inflammation in patients with inflammatory bowel disease.Journal of inflammation (London, England) · 2018Article
- Neisseria gonorrhoeae Lytic Transglycosylases LtgA and LtgD Reduce Host Innate Immune Signaling through TLR2 and NOD2.ACS infectious diseases · 2017Article
- The immunology of host defence peptides: beyond antimicrobial activity.Nature reviews. Immunology · 2016Review
- Cinobufagin Modulates Human Innate Immune Responses and Triggers Antibacterial Activity.PloS one · 2016Article
- Interrelatedness between dysbiosis in the gut microbiota due to immunodeficiency and disease penetrance of colitis.Immunology · 2015Review
- Debug Your Bugs - How NLRs Shape Intestinal Host-Microbe Interactions.Frontiers in immunology · 2013Review
- Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Interactions between Nod-Like Receptors and Intestinal Bacteria.Frontiers in immunology · 2013Review
- Cellular response to Trypanosoma cruzi infection induces secretion of defensin α-1, which damages the flagellum, neutralizes trypanosome motility, and inhibits infection.Infection and immunity · 2013Article
- IκB kinase α phosphorylation of TRAF4 downregulates innate immune signaling.Molecular and cellular biology · 2012Article
- A novel motif in the Crohn's disease susceptibility protein, NOD2, allows TRAF4 to down-regulate innate immune responses.The Journal of biological chemistry · 2011Article
- Toll-like receptors in inflammatory bowel diseases: a decade later.Inflammatory bowel diseases · 2010Review
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundHuman neutrophil peptide 1 (HNP-1) is a defensin with antibacterial activity secreted by various cells as a component of the innate immune host defense. NOD2 is a cytoplasmic protein that recognizes bacterial derived muramyl dipeptide, and is involved in bacterial clearance. The aim of the present study was to investigate the relationship between antibacterial activity of NOD2 and HNP-1 expression in epithelial cell lines.
methodsGentamicin protection assay using Salmonella typhimurium was performed in Caco-2 cells. The mRNA level was determined by quantitative reverse-transcription polymerase chain reaction (RT-PCR) and defensin expression was assessed by Western blot and enzyme-linked immunosorbent assay (ELISA). Nuclear factor-kappaB activation was assessed using pIV luciferase and Renilla plasmids. A NOD2 mutant was generated by site-directed mutagenesis.
resultsAmong the defensins tested, only HNP-1 expression is induced in colonic epithelial model HCT116 cells after MDP-LD stimulation. HNP-1 secretion is significantly increased after MDP-LD stimulation in the cell supernatant of intestinal epithelial cells expressing endogenous NOD2, but not in cells that lack endogenous NOD2 expression. HNP-1 is required for NOD2-dependent NF-kappaB activation after MDP-LD stimulation since hnp-1 siRNA transfection abrogated the response to MDP-LD stimulation. The antibacterial function of NOD2 against S. typhimurium was impaired when expression of HNP-1 was blocked by siRNA.
conclusionsHNP-1 secretion depends on NOD2 stimulation by MDP-LD and contributes to antibacterial activity in intestinal epithelial cells expressing endogenous NOD2, but not NOD2 3020insC mutant associated with increased susceptibility to Crohn's disease.
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