ArticleEnvironmental health perspectives2012
Hyaluronan activation of the Nlrp3 inflammasome contributes to the development of airway hyperresponsiveness.
Article in Environmental health perspectives, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 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
13 citing papers in PubMed, 21 citations in OpenAlex.
- Role of Damage-Associated Molecular Patterns (DAMPS) in the Postoperative Period after Colorectal Surgery.International journal of molecular sciences · 2023Review
- Modulation of hyaluronan signaling as a therapeutic target in human disease.Pharmacology & therapeutics · 2022Review
- Interleukin-1α Mediates Ozone-Induced Myeloid Differentiation Factor-88-Dependent Epithelial Tissue Injury and Inflammation.Frontiers in immunology · 2018Article
- Ozone-induced IL-17A and neutrophilic airway inflammation is orchestrated by the caspase-1-IL-1 cascade.Scientific reports · 2016Article
- Inflammasome, IL-1 and inflammation in ozone-induced lung injury.American journal of clinical and experimental immunology · 2016Review
- Novel Roles for Notch3 and Notch4 Receptors in Gene Expression and Susceptibility to Ozone-Induced Lung Inflammation in Mice.Environmental health perspectives · 2015Article
- Hyaluronan fragments as mediators of inflammation in allergic pulmonary disease.Immunobiology · 2015Review
- Size Matters: Molecular Weight Specificity of Hyaluronan Effects in Cell Biology.International journal of cell biology · 2015Review
- The Rise and Fall of Hyaluronan in Respiratory Diseases.International journal of cell biology · 2015Review
- Inflammasome Activity in Non-Microbial Lung Inflammation.Journal of environmental immunology and toxicology · 2014Article
- Investigating the role of nucleotide-binding oligomerization domain-like receptors in bacterial lung infection.American journal of respiratory and critical care medicine · 2014Review
- The NLRP3 inflammasome is required for the development of hypoxemia in LPS/mechanical ventilation acute lung injury.American journal of respiratory cell and molecular biology · 2014Article
- Exacerbated airway toxicity of environmental oxidant ozone in mice deficient in Nrf2.Oxidative medicine and cellular longevity · 2013Article
Corrections and comments
- Retraction · 2015-07-01Concerns/Issues about Data · Results Not Reproducible · · EN Potts-Kant aka EN Potts;
- Commented on by
- Retracted
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe role of the Nlrp3 inflammasome in nonallergic airway hyperresponsiveness (AHR) has not previously been reported. Recent evidence supports both interleukin (IL) 1β and short fragments of hyaluronan (HA) as contributors to the biological response to inhaled ozone.
objectiveBecause extracellular secretion of IL-1β requires activation of the inflammasome, we investigated the role of the inflammasome proteins ASC, caspase1, and Nlrp3 in the biological response to ozone and HA.
methodsC57BL/6J wild-type mice and mice deficient in ASC, caspase1, or Nlrp3 were exposed to ozone (1 ppm for 3 hr) or HA followed by analysis of airway resistance, cellular inflammation, and total protein and cytokines in bronchoalveolar lavage fluid (BALF). Transcription levels of IL-1β and IL-18 were determined in two populations of lung macrophages. In addition, we examined levels of cleaved caspase1 and cleaved IL-1β as markers of inflammasome activation in isolated alveolar macrophages harvested from BALF from HA-treated mice.
resultsWe observed that genes of the Nlrp3 inflammasome were required for development of AHR following exposure to either ozone or HA fragments. These genes are partially required for the cellular inflammatory response to ozone. The expression of IL-1β mRNA in alveolar macrophages was up-regulated after either ozone or HA challenge and was not dependent on the Nlrp3 inflammasome. However, soluble levels of IL-1β protein were dependent on the inflammasome after challenge with either ozone or HA. HA challenge resulted in cleavage of macrophage-derived caspase1 and IL-1β, suggesting a role for alveolar macrophages in Nlrp3-dependent AHR.
conclusionsThe Nlrp3 inflammasome is required for the development of ozone-induced reactive airways disease.
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.