The Metabolic Response to Ozone

Shore, Stephanie A.

doi:10.3389/fimmu.2019.02890

Cited by 23 publications

(12 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The adverse effect of O 3 on cardiovascular diseases has been also well established (Bourdrel et al 2017; Manisalidis et al 2020; Song et al 2020). However, the impact of this pollutant on metabolic alterations is less understood, even when the metabolic-impairment effects of O 3 have been determined in humans (Shore 2019). In this context, our results demonstrated that O 3 exposure had a significant effect on the regulation of the expression of certain adipokines and metabolic proteins that are linked to metabolic disease (i.e.…”

Section: Discussionmentioning

confidence: 99%

“…Extensive investigation about O 3 -related pathophysiological sequelae clearly show that exposure to this pollutant causes and exacerbates respiratory (D’Amato et al 2019; Manisalidis et al 2020; Sokolowska et al 2019) and cardiovascular diseases (Bourdrel et al 2017; Manisalidis et al 2020; Song et al 2020). What is more, O 3 exposure could also increase the incidence of chronic metabolic disorders, obesity and diabetes type II (Shore 2019; Thomson et al 2018), which has become one of the greatest global health threats of the 21st century. Furthermore, in humans, this pollutant increases the release of stress hormones, cortisol or rodent corticosterone (Thomson et al 2018), and alters the metabolic and endocrine response to the glucose challenge, which could also contribute to metabolic dysregulation (Thomson et al 2018).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of ozone exposure on Amyotrophic Lateral Sclerosis (ALS) pathology using a mice model of TDP-43 proteinopathy

Rodrı́guez¹,

Ferrer-Donato

Cabrera-Pinto

et al. 2021

Preprint

View full text Add to dashboard Cite

Background: Ozone (O3), one of the main photochemical pollutants in the atmosphere today, is a serious health risk factor. Although the effects of O3 exposure have been documented on many diseases, they have not yet been examined on Amyotrophic Lateral Sclerosis (ALS)- a fatal progressive and neurodegenerative disease. Objectives: To investigate the effect of the O3 exposure in a mice model of TDP-43 proteinopathy, exploring a possible association between the O3 exposure and the ALS pathogenesis. Methods: TDP-43A315T and wild-type (WT) mice were exposed to O3 (0.25 ppm) or filtered air (FA) for 15 days (4 hours/day). We assessed (1) weight loss (2) motor performance (3) plasma glucose content and (4) metabolic markers from plasma samples of the animals. Results: Throughout the experiment, we observed a progressive decline in body weight and the motor coordination in TDP-43A315T mice compared to WT controls. Although there was a trend, there were no significant differences in the decline of body weight of TDP-43A315T mice when exposed to either FA or O3. In O3-TDP-43A315T mice, the disease duration lasted longer. In addition, O3-TDP-43A315T mice showed improvements in motor performance as well TDP-43A315T mice were hypoglycemic compared to WT mice. However, FA-TDP-43A315T mice showed lower plasma glucose levels at the disease end-stage. We found altered levels of adipokines and metabolic proteins in TDP-43A315T mice compared to WT controls. A positive correlation was found among GIP and glucagon compared to insulin concentrations in control mice. Interestingly, resistin, Gastric Inhibitory Peptide (GIP), Glucagon Like Peptide 1 (GIP-1) and insulin levels were higher in O3-TDP-43A315T mice. Discussion: We provide new evidence about a mechanistic link between O3 exposure and the improvement of the metabolic disturbances present in TDP-43A315T mice. Further studies are needed to corroborate the obtained results as they warrant to understanding the underlying mechanisms.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of ozone exposure on Amyotrophic Lateral Sclerosis (ALS) pathology using a mice model of TDP-43 proteinopathy

Rodrı́guez¹,

Ferrer-Donato

Cabrera-Pinto

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…O 3 exposure-released adrenal-derived stress hormones (e.g., epinephrine and corticosterone) disrupted lipid and carbohydrate metabolism, leading to hyperglycemia, glucose intolerance, and lung injury in rats [ 61 , 62 ]. Further rodent studies demonstrated that obesity augmented acute O 3 -induced airway hyperresponsiveness and inflammation [ 63 , 64 , 65 ], and diabetes caused early and exacerbated lung inflammation and fibrotic changes in response to subchronic O 3 (0.5 ppm, 4 h/day for 13 weeks) [ 10 ]. Epidemiological studies also showed a positive association between O 3 exposure and adult insulin resistance and preexisting lipid disorders and metabolic conditions (e.g., obesity and diabetes) [ 66 , 67 , 68 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptomics Underlying Pulmonary Ozone Pathogenesis Regulated by Inflammatory Mediators in Mice

et al. 2021

View full text Add to dashboard Cite

Ozone (O3) is the predominant oxidant air pollutant associated with airway inflammation, lung dysfunction, and the worsening of preexisting respiratory diseases. We previously demonstrated the injurious roles of pulmonary immune receptors, tumor necrosis factor receptor (TNFR), and toll-like receptor 4, as well as a transcription factor NF-κB, in response to O3 in mice. In the current study, we profiled time-dependent and TNFR- and NF-κB-regulated lung transcriptome changes by subacute O3 to illuminate the underlying molecular events and downstream targets. Mice lacking Tnfr1/Tnfr2 (Tnfr-/-) or Nfkb1 (Nfkb1-/-) were exposed to air or O3. Lung RNAs were prepared for cDNA microarray analyses, and downstream and upstream mechanisms were predicted by pathway analyses of the enriched genes. O3 significantly altered the genes involved in inflammation and redox (24 h), cholesterol biosynthesis and vaso-occlusion (48 h), and cell cycle and DNA repair (48–72 h). Transforming growth factor-β1 was a predicted upstream regulator. Lack of Tnfr suppressed the immune cell proliferation and lipid-related processes and heightened epithelial cell integrity, and Nfkb1 deficiency markedly suppressed lung cell cycle progress during O3 exposure. Common differentially regulated genes by TNFR and NF-κB1 (e.g., Casp8, Il6, and Edn1) were predicted to protect the lungs from cell death, connective tissue injury, and inflammation. Il6-deficient mice were susceptible to O3-induced protein hyperpermeability, indicating its defensive role, while Tnf-deficient mice were resistant to overall lung injury caused by O3. The results elucidated transcriptome dynamics and provided new insights into the molecular mechanisms regulated by TNFR and NF-κB1 in pulmonary subacute O3 pathogenesis.

show abstract

“…4 Air pollutants are known to cause inflammatory changes in respiratory epithelium and the impact of ambient air pollution on CRS pathogenesis and progression has recently been receiving increasing attention. [4][5][6][7][8][9][10][11] However, to our knowledge, the association between common air pollutants and sinonasal histopathology in CRS patients have not been studied thus far.…”

Section: Introductionmentioning

confidence: 99%

Association of Air Pollutant Exposure and Sinonasal Histopathology Findings in Chronic Rhinosinusitis

Patel

Tajudeen

Brown

et al. 2021

Am J Rhinol�Allergy

View full text Add to dashboard Cite

Background Ambient air pollution is well known to cause inflammatory change in respiratory epithelium and is associated with exacerbations of inflammatory conditions such as asthma and chronic obstructive pulmonary disease. However, limited work has been done on the impact of air pollution on pathogenesis of chronic rhinosinusitis and there are no reports in the literature of how pollutant exposure may impact sinonasal histopathology in patients with chronic rhinosinusitis. Objective This study aims to identify associations between certain histopathologic characteristics seen in sinus tissue of patients with chronic rhinosinusitis (CRS) and levels of particulate air pollution (PM2.5) and ground-level ozone in their place of residence. Methods A structured histopathology report was created to characterize the tissues of CRS patients undergoing sinus surgery. An estimate for each patient’s exposure to air pollutants including small particulate matter (PM2.5) and ground-level ozone was obtained using the Environmental Protection Agency’s (EPA) Environmental Justice Screening and Mapping Tool (EJSCREEN). Mean pollutant exposures for patients whose tissues exhibited varying histopathologic features were compared using logistic regression models. Results Data from 291 CRS patients were analyzed. Higher degree of inflammation was significantly associated with increased ozone exposure (p = 0.031). Amongst the patients with CRSwNP (n=131), presence of eosinophilic aggregates (p = 0.018) and Charcot-Leyden crystals (p = 0.036) was associated with increased ozone exposure. Conclusion Exposure to ambient air pollutants may contribute to pathogenesis of CRS. Increasing ozone exposure was linked to both higher tissue inflammation and presence of eosinophilic aggregates and Charcot-Leyden crystals in CRSwNP patients.

show abstract

The Metabolic Response to Ozone

Cited by 23 publications

References 72 publications

Effect of ozone exposure on Amyotrophic Lateral Sclerosis (ALS) pathology using a mice model of TDP-43 proteinopathy

Effect of ozone exposure on Amyotrophic Lateral Sclerosis (ALS) pathology using a mice model of TDP-43 proteinopathy

Transcriptomics Underlying Pulmonary Ozone Pathogenesis Regulated by Inflammatory Mediators in Mice

Association of Air Pollutant Exposure and Sinonasal Histopathology Findings in Chronic Rhinosinusitis

Contact Info

Product

Resources

About