ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014
Pivotal role of IL-6 in the hyperinflammatory responses to subacute ozone in adiponectin-deficient mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Non-type 2 airway inflammation in severe asthma: from bench to bedside.Frontiers in immunology · 2026Review
- ALX/FPR2 Contributes to Serum Amyloid A-Induced Lung Neutrophil Recruitment Following Acute Ozone Exposure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Decoding mechanisms and protein markers in lung-brain axis.Respiratory research · 2025Review
- Effects of Ozone on Sickness and Depressive-like Behavioral and Biochemical Phenotypes and Their Regulation by Serum Amyloid A in Mice.International journal of molecular sciences · 2023Article
- Ozone-Induced Oxidative Stress, Neutrophilic Airway Inflammation, and Glucocorticoid Resistance in Asthma.Frontiers in immunology · 2021Review
- Characterization of low-dose ozone-induced murine acute lung injury.Physiological reports · 2020Article
- The interleukin-33 receptor contributes to pulmonary responses to ozone in male mice: role of the microbiome.Respiratory research · 2019Article
- Augmented Responses to Ozone in Obese Mice Require IL-17A and Gastrin-Releasing Peptide.American journal of respiratory cell and molecular biology · 2018Article
- Mechanistic Basis for Obesity-related Increases in Ozone-induced Airway Hyperresponsiveness in Mice.Annals of the American Thoracic Society · 2017Review
- Serum amyloid A: an ozone-induced circulating factor with potentially important functions in the lung-brain axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- IL-33 Drives Augmented Responses to Ozone in Obese Mice.Environmental health perspectives · 2017Article
- Article
- Repeated Mouse Lung Exposures to Stachybotrys chartarum Shift Immune Response from Type 1 to Type 2.American journal of respiratory cell and molecular biology · 2016Article
- Effects of mannose-binding lectin on pulmonary gene expression and innate immune inflammatory response to ozone.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Regulation of IL-17A expression in mice following subacute ozone exposure.Journal of immunotoxicology · 2016Article
- Mechanisms of Asthma in Obesity. Pleiotropic Aspects of Obesity Produce Distinct Asthma Phenotypes.American journal of respiratory cell and molecular biology · 2016Review
- Inflammasome, IL-1 and inflammation in ozone-induced lung injury.American journal of clinical and experimental immunology · 2016Review
- Immunological characteristics and management considerations in obese patients with asthma.Expert review of clinical immunology · 2015Review
- γδ T Cells Are Required for M2 Macrophage Polarization and Resolution of Ozone-Induced Pulmonary Inflammation in Mice.PloS one · 2015Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Adiponectin is an adipose-derived hormone with anti-inflammatory activity. Following subacute ozone exposure (0.3 ppm for 24-72 h), neutrophilic inflammation and IL-6 are augmented in adiponectin-deficient (Adipo(-/-)) mice. The IL-17/granulocyte colony-stimulating factor (G-CSF) axis is required for this increased neutrophilia. We hypothesized that elevated IL-6 in Adipo(-/-) mice contributes to their augmented responses to ozone via effects on IL-17A expression. Therefore, we generated mice deficient in both adiponectin and IL-6 (Adipo(-/-)/IL-6(-/-)) and exposed them to ozone or air. In ozone-exposed mice, bronchoalveolar lavage (BAL) neutrophils, IL-6, and G-CSF, and pulmonary Il17a mRNA expression were greater in Adipo(-/-) vs. wild-type mice, but reduced in Adipo(-/-)/IL-6(-/-) vs. Adipo(-/-) mice. IL-17A(+) F4/80(+) cells and IL-17A(+) γδ T cells were also reduced in Adipo(-/-)/IL-6(-/-) vs. Adipo(-/-) mice exposed to ozone. Only BAL neutrophils were reduced in IL-6(-/-) vs. wild-type mice. In wild-type mice, IL-6 was expressed in Gr-1(+)F4/80(-)CD11c(-) cells, whereas in Adipo(-/-) mice F4/80(+)CD11c(+) cells also expressed IL-6, suggesting that IL-6 is regulated by adiponectin in these alveolar macrophages. Transcriptomic analysis identified serum amyloid A3 (Saa3), which promotes IL-17A expression, as the gene most differentially augmented by ozone in Adipo(-/-) vs. wild-type mice. After ozone, Saa3 mRNA expression was markedly greater in Adipo(-/-) vs. wild-type mice but reduced in Adipo(-/-)/IL-6(-/-) vs. Adipo(-/-) mice. In conclusion, our data support a pivotal role of IL-6 in the hyperinflammatory condition observed in Adipo(-/-) mice after ozone exposure and suggest that this role of IL-6 involves its ability to induce Saa3, IL-17A, and G-CSF.
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Registered trials
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