ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Cutting edge: Crohn's disease-associated Nod2 mutation limits production of proinflammatory cytokines to protect the host from Enterococcus faecalis-induced lethality.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 59 citations in OpenAlex.
- Effects and Molecular Mechanisms of Heat-Killed PostbioticInternational journal of molecular sciences · 2026Article
- Monogenic disorders of immunity: Common variants are not so rare.Cell genomics · 2026Review
- The complement system in intestinal inflammation and cancer.The Journal of clinical investigation · 2025Review
- Autophagy and Bacterial infections.Autophagy reports · 2025Review
- Fibrostenosing Crohn's Disease: Pathogenetic Mechanisms and New Therapeutic Horizons.International journal of molecular sciences · 2024Review
- Role and molecular mechanism of NOD2 in chronic non-communicable diseases.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Article
- Antimicrobial overproduction sustains intestinal inflammation by inhibiting Enterococcus colonization.Cell host & microbe · 2023Article
- Ileocolonic Healing after Small Ileocecal Resection in Mice: NOD2 Deficiency Impairs Anastomotic Healing by Local Mechanisms.Journal of clinical medicine · 2023Article
- Multifaceted roles and regulation of nucleotide-binding oligomerization domain containing proteins.Frontiers in immunology · 2023Review
- NOD1 and NOD2 in inflammatory and infectious diseases.Immunological reviews · 2020Review
- Review
- A specific gene-microbe interaction drives the development of Crohn's disease-like colitis in mice.Science immunology · 2019Article
- B Cell Defects Observed inJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- Alterations in nucleotide-binding oligomerization domain-2 expression, pathway activation, and cytokine production in Yao syndrome.Autoimmunity · 2018Article
- NOD2 and inflammation: current insights.Journal of inflammation research · 2018Review
- NOD1 and NOD2: Beyond Peptidoglycan Sensing.Trends in immunology · 2017Review
- Understanding the regulation of pattern recognition receptors in inflammatory diseases - a 'Nod' in the right direction.Immunology · 2017Review
- Mechanisms of Intestinal Epithelial Barrier Dysfunction by Adherent-InvasiveCellular and molecular gastroenterology and hepatology · 2017Review
- Gram-Positive Uropathogens, Polymicrobial Urinary Tract Infection, and the Emerging Microbiota of the Urinary Tract.Microbiology spectrum · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Nucleotide-binding oligomerization domain 2 (Nod2) mutations including L1007fsinsC are associated with the development of Crohn's disease (CD). These CD-associated Nod2 mutations are common in healthy white populations, suggesting that they may confer some protective function, but experimental evidence is lacking. Using a mouse strain that expresses Nod2(2939iCstop), the equivalent of the L1007fsinsC mutation, we found that macrophages homozygous for Nod2(2939iCstop) are impaired in the recognition of muramyl dipeptide and Enterococcus faecalis, a commensal bacterium that is a common cause of sepsis-associated lethality in humans. Notably, Nod2 deficiency and homozygocity for Nod2(2939iCstop) were associated with reduced production of TNF-α and IL-6 and lethality after systemic infection with E. faecalis despite normal bacteria loads. Consistently, inhibition of TNF-α signaling protected wild-type mice from E. faecalis-induced lethality. These results suggest that the same Nod2 mutation can increase the susceptibility to CD, but also protect the host from systemic infection by a common enteric bacterium.
Indexed as
Identifiers
What OpenQuestion holds
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.