ArticleAmerican journal of respiratory and critical care medicine2009
Toll-like receptor 2 is essential for the sensing of oxidants during inflammation.
Article in American journal of respiratory and critical care medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed, 57 citations in OpenAlex.
- A peripheral subpopulation of retinal pigment epithelium resists oxidative damage through SERPINE3-mediated caspase-1 inhibition.The Journal of clinical investigation · 2026Article
- PM2.5 Exposure and Asthma Development: The Key Role of Oxidative Stress.Oxidative medicine and cellular longevity · 2022Review
- Exogenous oxidants activate nuclear factor kappa B through Toll-like receptor 4 stimulation to maintain inflammatory phenotype in macrophage.Biochemical pharmacology · 2018Article
- Article
- Phagocytosis and Inflammation: Exploring the effects of the components of E-cigarette vapor on macrophages.Physiological reports · 2017Article
- Intermedin attenuates renal fibrosis by induction of heme oxygenase-1 in rats with unilateral ureteral obstruction.BMC nephrology · 2017Article
- TLR2 and TLR9 modulate enteric nervous system inflammatory responses to lipopolysaccharide.Journal of neuroinflammation · 2016Article
- Article
- Molecular processes that drive cigarette smoke-induced epithelial cell fate of the lung.American journal of respiratory cell and molecular biology · 2014Review
- TLR2, TLR3, and TLR4 activation specifically alters the oxidative status of intestinal epithelial cells.Cell stress & chaperones · 2014Article
- Are reactive oxygen species always detrimental to pathogens?Antioxidants & redox signaling · 2014Review
- β2-Adrenoceptor involved in smoking-induced airway mucus hypersecretion through β-arrestin-dependent signaling.PloS one · 2014Article
- Toll-like receptors in atherosclerosis.International journal of molecular sciences · 2013Review
- Article
- Innate immune function by Toll-like receptors: distinct responses in newborns and the elderly.Immunity · 2012Review
- Use of xanthine oxidase inhibitor febuxostat inhibits renal interstitial inflammation and fibrosis in unilateral ureteral obstructive nephropathy.Clinical and experimental nephrology · 2012Article
- Toll-like receptor genes and their association with colon and rectal cancer development and prognosis.International journal of cancer · 2012Article
- Role of reactive oxygen and nitrogen species in the vascular responses to inflammation.Free radical biology & medicine · 2012Review
- Inflammatory transcriptome profiling of human monocytes exposed acutely to cigarette smoke.PloS one · 2012Article
- Glaucomatous tissue stress and the regulation of immune response through glial Toll-like receptor signaling.Investigative ophthalmology & visual science · 2010Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
rationaleThe mechanisms by which oxidants are sensed by cells and cause inflammation are not well understood.
objectivesThis study aimed to determine how cells "sense" soluble oxidants and how this is translated into an inflammatory reaction.
methodsMonocytes, macrophages, or HEK293 cells (stably transfected with human Toll-like receptor [TLR]2, TLR2/1, TLR2/6, or TLR4/MD2-CD14) were used. CXC ligand-8 (CXCL8) levels were measured using ELISA. Phosphorylated IL-1 receptor-associated kinase 1 levels were measured using Western blot. TLR2(-/-) and TLR4(-/-) mice were challenged with oxidants, and inflammation was measured by monitoring cell infiltration and KC levels. MEASUREMENTS AND MAIN
resultsOxidants evoked the release of CXCL8 from monocytes/macrophages; this was abrogated by pretreatment with N-acetylcysteine or binding antibodies to TLR2 and was associated with the rapid phosphorylation of IL-1 receptor-associated kinase 1. Oxidants added to HEK293 cells transfected with TLR2, TLR1/2, or TLR2/6 but not TLR4/MD2-CD14 or control HEK nulls resulted in the release of CXCL8. Oxidant challenge delivered intraperitoneally (2-24 hours) or by inhalation to the lungs (3 days) resulted in a robust inflammation in wild-type mice. TLR2(-/-) mice did not respond to oxidant challenge in either model. TLR4(-/-) mice responded as wild-type mice to oxidants at 2 hours but as TLR2(-/-) mice at later time points.
conclusionsOxidant-TLR2 interactions provide a signal that initiates the inflammatory response.
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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.