ArticleThe Journal of biological chemistry2010
A novel pathway for inducible nitric-oxide synthase activation through inflammasomes.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 55 citations in OpenAlex.
- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- Reactive oxygen species and reactive nitrogen species are double-edged swords in Salmonella infection.Archives of microbiology · 2025Review
- "Just right" combinations of adjuvants with nanoscale carriers activate aged dendritic cells without overt inflammation.Immunity & ageing : I & A · 2023Article
- NAIP/NLRC4 inflammasome participates in macrophage responses toFrontiers in immunology · 2023Article
- Lysosomal cathepsins act in concert with Gasdermin-D during NAIP/NLRC4-dependent IL-1β secretion.Cell death & disease · 2022Article
- Inflammasomes and Colorectal Cancer.Cells · 2021Review
- TLR5 activation in hepatocytes alleviates the functional suppression of intrahepatic CD8Immunology · 2020Article
- São Paulo School of Advanced Sciences on Vaccines: an overview.The journal of venomous animals and toxins including tropical diseases · 2020Review
- Transcriptomic Profiles of Monocyte-Derived Macrophages in Response to Escherichia coli is Associated with the Host Genetics.Scientific reports · 2020Article
- Porcine Alveolar Macrophages' Nitric Oxide Synthase-Mediated Generation of Nitric Oxide Exerts Important Defensive Effects againstPathogens (Basel, Switzerland) · 2019Article
- Epigenetic regulation of nitric oxide synthase 2, inducible (Nos2) by NLRC4 inflammasomes involves PARP1 cleavage.Scientific reports · 2017Article
- Post-translational regulation of inflammasomes.Cellular & molecular immunology · 2017Review
- Article
- Over-activation of TLR5 signaling by high-dose flagellin induces liver injury in mice.Cellular & molecular immunology · 2015Article
- Shedding of the tumor necrosis factor (TNF) receptor from the surface of hepatocytes during sepsis limits inflammation through cGMP signaling.Science signaling · 2015Article
- Redundant and cooperative interactions between TLR5 and NLRC4 in protective lung mucosal immunity against Pseudomonas aeruginosa.Journal of innate immunity · 2015Article
- Flagellins of Salmonella Typhi and nonpathogenic Escherichia coli are differentially recognized through the NLRC4 pathway in macrophages.Journal of innate immunity · 2014Article
- Article
- Emerging Concepts about NAIP/NLRC4 Inflammasomes.Frontiers in immunology · 2014Review
- Cytosolic flagellin-induced lysosomal pathway regulates inflammasome-dependent and -independent macrophage responses.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Innate immune recognition of flagellin is shared by transmembrane TLR5 and cytosolic Nlrc4 (NOD-like receptor family CARD (caspase activation recruitment domain) domain containing 4)/Naip5 (neuronal apoptosis inhibitory protein 5). TLR5 activates inflammatory genes through MYD88 pathway, whereas Nlrc4 and Naip5 assemble multiprotein complexes called inflammasomes, culminating in caspase-1 activation, IL-1β/IL-18 secretion, and pyroptosis. Although both TLR5 and Naip5/Nlrc4 pathways cooperate to clear infections, little is known about the relative anti-pathogen effector mechanisms operating through each of them. Here we show that the cytosolic flagellin (FLA-BSDot) was able to activate iNOS, an enzyme previously associated with TLR5 pathway. Using Nlrc4- or Naip5-deficient macrophages, we found that both receptors are involved in iNOS activation by FLA-BSDot. Moreover, distinct from extracellular flagellin (FLA-BS), iNOS activation by intracellular flagellin is completely abrogated in the absence of caspase-1. Interestingly, IL-1β and IL-18 do not seem to be important for FLA-BSDot-mediated iNOS production. Together, our data defined an additional anti-pathogen effector mechanism operated through Naip5 and Nlrc4 inflammasomes and illustrated a novel signaling transduction pathway that activates iNOS.
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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.