ArticleAmerican journal of respiratory cell and molecular biology2007
Type I interleukin-1 receptor is required for pulmonary responses to subacute ozone exposure in mice.
Article in American journal of respiratory cell and molecular biology, 2007. 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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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.
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Who cites it
28 citing papers in PubMed, 38 citations in OpenAlex.
- Tristetraprolin protects against ozone-induced acute lung injury and inflammation in mice.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Interleukin-11 receptor subunit α-1 is required for maximal airway responsiveness to methacholine after acute exposure to ozone.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Transcriptional Profiling of the Murine Airway Response to Acute Ozone Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Functional and morphological differences of the lung upon acute and chronic ozone exposure in mice.Scientific reports · 2018Article
- Curcumin Exerted Neuroprotection against Ozone-Induced Oxidative Damage and Decreased NF-Oxidative medicine and cellular longevity · 2018Article
- Interleukin-1α Mediates Ozone-Induced Myeloid Differentiation Factor-88-Dependent Epithelial Tissue Injury and Inflammation.Frontiers in immunology · 2018Article
- Chemokine (C-C Motif) Receptor-Like 2 is not essential for lung injury, lung inflammation, or airway hyperresponsiveness induced by acute exposure to ozone.Physiological reports · 2017Article
- Role of ROCK2 in CD4Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2017Article
- Regulation of IL-17A expression in mice following subacute ozone exposure.Journal of immunotoxicology · 2016Article
- Group 2 innate lymphoid cells mediate ozone-induced airway inflammation and hyperresponsiveness in mice.The Journal of allergy and clinical immunology · 2016Article
- 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
- Resistin deficiency in mice has no effect on pulmonary responses induced by acute ozone exposure.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Sex differences in the expression of lung inflammatory mediators in response to ozone.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- The IL-1 axis is associated with airway inflammation after O3 exposure in allergic asthmatic patients.The Journal of allergy and clinical immunology · 2015Article
- Ozone exposure initiates a sequential signaling cascade in airways involving interleukin-1beta release, nerve growth factor secretion, and substance P upregulation.Journal of toxicology and environmental health. Part A · 2015Article
- Endogenous osteopontin promotes ozone-induced neutrophil recruitment to the lungs and airway hyperresponsiveness to methacholine.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Hyaluronan activation of the Nlrp3 inflammasome contributes to the development of airway hyperresponsiveness.Environmental health perspectives · 2012Article
- Pulmonary inflammation induced by subacute ozone is augmented in adiponectin-deficient mice: role of IL-17A.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Impact of aging on pulmonary responses to acute ozone exposure in mice: role of TNFR1.Inhalation toxicology · 2011Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Interleukin (IL)-1, a proinflammatory cytokine, is expressed in the lung after ozone (O(3)) exposure. IL-1 mediates its effects through the type I IL-1 receptor (IL-1RI), the only signaling receptor for both IL-1alpha and IL-1beta. The purpose of this study was to determine the role of IL-1RI in pulmonary responses to O(3.) To that end, wild-type, C57BL/6 (IL-1RI(+/+)) mice and IL-1RI-deficient (IL-1RI(-/-)) mice were exposed to O(3) either subacutely (0.3 ppm for 72 h) or acutely (2 ppm for 3 h). Subacute O(3) exposure increased bronchoalveolar lavage fluid (BALF) protein, interferon-gamma-inducible protein (IP)-10, soluble tumor necrosis factor receptor 1 (sTNFR1), and neutrophils in IL-1RI(+/+) and IL-1RI(-/-) mice. With the exception of IP-10, all outcome indicators were reduced in IL-1RI(-/-) mice. Furthermore, subacute O(3) exposure increased IL-6 mRNA expression in IL-1RI(+/+), but not IL-1RI(-/-) mice. Acute (2 ppm) O(3) exposure increased BALF protein, IL-6, eotaxin, KC, macrophage inflammatory protein (MIP)-2, IP-10, monocyte chemotactic protein-1, sTNFR1, neutrophils, and epithelial cells in IL-1RI(+/+) and IL-1RI(-/-) mice. For IL-6, eotaxin, MIP-2, and sTNFR1, there were small but significant reductions of these outcome indicators in IL-1RI(-/-) versus IL-1RI(+/+) mice at 6 hours after exposure, but not at other time points, whereas other outcome indicators were unaffected by IL-1RI deficiency. These results suggest that IL-1RI is required for O(3)-induced pulmonary inflammation during subacute O(3) exposure, but plays a more minor role during acute O(3) exposure. In addition, these results suggest that the induction of IL-6 via IL-1RI may be important in mediating the effects of O(3) during subacute exposure.
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