ArticlePloS one2010
Direct bacterial killing in vitro by recombinant Nod2 is compromised by Crohn's disease-associated mutations.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Paneth cells as orchestrators of epithelial barrier defense and emerging therapeutic targets in inflammatory bowel disease.Seminars in immunopathology · 2026Review
- Is hidradenitis suppurativa more an autoinfection than pure autoinflammation?Frontiers in immunology · 2026Review
- RAIN: machine learning-based identification for HIV-1 bNAbs.Nature communications · 2024Article
- An Update Review on the Paneth Cell as Key to Ileal Crohn's Disease.Frontiers in immunology · 2020Review
- The Bacterial Peptidoglycan-Sensing Molecules NOD1 and NOD2 Promote CD8Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- 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
- The c-Jun N-terminal kinase (JNK)-binding protein (JNKBP1) acts as a negative regulator of NOD2 protein signaling by inhibiting its oligomerization process.The Journal of biological chemistry · 2012Article
- NOD2 signaling contributes to host defense in the lungs against Escherichia coli infection.Infection and immunity · 2012Article
- Inflammation drives dysbiosis and bacterial invasion in murine models of ileal Crohn's disease.PloS one · 2012Article
- Host genetics and environmental factors regulate ecological succession of the mouse colon tissue-associated microbiota.PloS one · 2012Article
- The role of bacteria and pattern-recognition receptors in Crohn's disease.Nature reviews. Gastroenterology & hepatology · 2011Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA homeostatic relationship with the intestinal microflora is increasingly appreciated as essential for human health and wellbeing. Mutations in the leucine-rich repeat (LRR) domain of Nod2, a bacterial recognition protein, are associated with development of the inflammatory bowel disorder, Crohn's disease. We investigated the molecular mechanisms underlying disruption of intestinal symbiosis in patients carrying Nod2 mutations. METHODOLOGY/PRINCIPAL
findingsIn this study, using purified recombinant LRR domains, we demonstrate that Nod2 is a direct antimicrobial agent and this activity is generally deficient in proteins carrying Crohn's-associated mutations. Wild-type, but not Crohn's-associated, Nod2 LRR domains directly interacted with bacteria in vitro, altered their metabolism and disrupted the integrity of the plasma membrane. Antibiotic activity was also expressed by the LRR domains of Nod1 and other pattern recognition receptors suggesting that the LRR domain is a conserved anti-microbial motif supporting innate cellular immunity. CONCLUSIONS/SIGNIFICANCE: The lack of anti-bacterial activity demonstrated with Crohn's-associated Nod2 mutations in vitro, supports the hypothesis that a deficiency in direct bacterial killing contributes to the association of Nod2 polymorphisms with the disease.
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Registered trials
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