ArticleJournal of leukocyte biology2015
Role for NOD2 in Mycobacterium tuberculosis-induced iNOS expression and NO production in human macrophages.
Article in Journal of leukocyte biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- The influence of single nucleotide polymorphisms of NOD2 or CD14 on the risk of Mycobacterium tuberculosis diseases: a systematic review.Systematic reviews · 2021Pooled it
- T cell-macrophage interactions in tuberculosis: What we've got here is failure to communicate.Journal of internal medicine · 2026Review
- Genomic insights into ancestry and infectious disease in 17th-century colonial Brazil.bioRxiv : the preprint server for biology · 2025Article
- Desmuramylpeptide, a NOD2 agonist, enhanced immune response and parasite clearance inFuture medicinal chemistry · 2025Article
- Article
- ZDHHC2 promoted antimycobacterial responses by selective autophagic degradation of B-RAF and C-RAF in macrophages.Science advances · 2025Article
- Article
- A nod to paratuberculosis: NOD1 and NOD2 expression in the pathological spectrum ofFrontiers in veterinary science · 2025Article
- Improvement effects of cyclic peptides fromFood science and biotechnology · 2024Article
- Muramyl dipeptide potentiatesFrontiers in immunology · 2024Article
- A nod to the bond between NOD2 and mycobacteria.PLoS pathogens · 2023Review
- Immunomodulatory Activity of Diterpenes over Innate Immunity and Cytokine Production in a Human Alveolar Epithelial Cell Line Infected withCurrent molecular pharmacology · 2023Article
- Review
- IFN-γ-mediated control of SARS-CoV-2 infection through nitric oxide.Frontiers in immunology · 2023Article
- Review
- In-depth systems biological evaluation of bovine alveolar macrophages suggests novel insights into molecular mechanisms underlyingFrontiers in microbiology · 2022Article
- Type I Interferons Are Involved in the Intracellular Growth Control ofFrontiers in immunology · 2021Article
- Article
- Underwhelming or Misunderstood? Genetic Variability of Pattern Recognition Receptors in Immune Responses and Resistance toFrontiers in immunology · 2021Review
- Mutual alteration of NOD2-associated Blau syndrome and IFNγR1 deficiency.Journal of clinical immunology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
M.tb, which causes TB, is a host-adapted intracellular pathogen of macrophages. Macrophage intracellular PRRs, such as NOD proteins, regulate proinflammatory cytokine production in response to various pathogenic organisms. We demonstrated previously that NOD2 plays an important role in controlling the inflammatory response and viability of M.tb and Mycobacterium bovis BCG in human macrophages. Various inflammatory mediators, such as cytokines, ROS, and RNS, such as NO, can mediate this control. iNOS (or NOS2) is a key enzyme for NO production and M.tb control during infection of mouse macrophages; however, the role of NO during infection of human macrophages remains unclear, in part, as a result of the low amounts of NO produced in these cells. Here, we tested the hypothesis that activation of NOD2 by its ligands (MDP and GMDP, the latter from M.tb) plays an important role in the expression and activity of iNOS and NO production in human macrophages. We demonstrate that M.tb or M. bovis BCG infection enhances iNOS expression in human macrophages. The M.tb-induced iNOS expression and NO production are dependent on NOD2 expression during M.tb infection. Finally, NF-κB activation is required for NOD2-dependent expression of iNOS in human macrophages. Our data provide evidence for a new molecular pathway that links activation of NOD2, an important intracellular PRR, and iNOS expression and activity during M.tb infection of human macrophages.
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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.