Diesel exhaust exposure intensifies inflammatory and structural changes associated with lung aging in mice

Júnior, Gabriel Ribeiro; Costa, Natália; Belotti, Luciano; Alemany, Adair Aparecida dos Santos; Amato-Lourenço, Luís Fernando; Cunha, Paula Gabriela da; Duro, Stephanie de Oliveira; Ribeiro, Susan Pereira; Veras, Mariana Matera; Lopes, Fernanda Degobbi Tenório Quirino dos Santos; Marcourakis, Tânia; Saldiva, Paulo Hilário Nascimento; Farsky, Sandra Helena Poliselli; Mauad, Thaís

doi:10.1016/j.ecoenv.2018.11.139

Cited by 15 publications

(5 citation statements)

References 36 publications

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“…Both Gpx-1/2 and catalase expression levels were increased in response to DEP exposure, which could be fully prevented by DMF treatment (Figure 4). Interestingly, a recent study in young mice demonstrated no effect of diesel exhaust exposure (30 days) on Gpx activity in lung tissue [46]. Based on our findings, it is conceivable that both GPx-1/2 and catalase were upregulated in defense against the oxidative stress promoted by DEP exposure (evidenced by ROS, ONOO and NO; Table 1).…”

Section: Discussionsupporting

confidence: 64%

“…DEP exposure alone did not change the expression of SOD-1, while DMF treatment of DEP-exposed mice reduced its expression below control levels. Conversely, mice exposed to diesel exhaust for 30 days showed an elevation of SOD activity in lung tissue [46]. It is feasible that because of its role as the first enzyme acting against ROS, SOD-1 expression after 60 days of exposure was already reduced because of the progressed lung response (i.e., antioxidant system moved on to the next step) against the prolonged oxidative stress promoted by DEP.…”

Section: Discussionmentioning

confidence: 99%

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Dimethyl Fumarate Attenuates Lung Inflammation and Oxidative Stress Induced by Chronic Exposure to Diesel Exhaust Particles in Mice

Cattani‐Cavalieri

Valença

Moraes

et al. 2020

IJMS

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Air pollution is mainly caused by burning of fossil fuels, such as diesel, and is associated with increased morbidity and mortality due to adverse health effects induced by inflammation and oxidative stress. Dimethyl fumarate (DMF) is a fumaric acid ester and acts as an antioxidant and anti-inflammatory agent. We investigated the potential therapeutic effects of DMF on pulmonary damage caused by chronic exposure to diesel exhaust particles (DEPs). Mice were challenged with DEPs (30 μg per mice) by intranasal instillation for 60 consecutive days. After the first 30 days, the animals were treated daily with 30 mg/kg of DMF by gavage for the remainder of the experimental period. We demonstrated a reduction in total inflammatory cell number in the bronchoalveolar lavage (BAL) of mice subjected to DEP + DMF as compared to those exposed to DEPs alone. Importantly, DMF treatment was able to reduce lung injury caused by DEP exposure. Intracellular total reactive oxygen species (ROS), peroxynitrite (OONO), and nitric oxide (NO) levels were significantly lower in the DEP + DMF than in the DEP group. In addition, DMF treatment reduced the protein expression of kelch-like ECH-associated protein 1 (Keap-1) in lung lysates from DEP-exposed mice, whereas total nuclear factor κB (NF-κB) p65 expression was decreased below baseline in the DEP + DMF group compared to both the control and DEP groups. Lastly, DMF markedly reduced DEP-induced expression of nitrotyrosine, glutathione peroxidase-1/2 (Gpx-1/2), and catalase in mouse lungs. In summary, DMF treatment effectively reduced lung injury, inflammation, and oxidative and nitrosative stress induced by chronic DEP exposure. Consequently, it may lead to new therapies to diminish lung injury caused by air pollutants.

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Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Dimethyl Fumarate Attenuates Lung Inflammation and Oxidative Stress Induced by Chronic Exposure to Diesel Exhaust Particles in Mice

Cattani‐Cavalieri

Valença

Moraes

et al. 2020

IJMS

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“…In young animals, lung SIRT6 gene expression was decreased, while protein expression increased. No effects in SIRT6 were observed in old animals ( Ribeiro Júnior et al, 2019 ).…”

Section: Antagonistic Hallmarks Of Aging–mitochondrial Dysfunction De...mentioning

confidence: 92%

Aging, longevity, and the role of environmental stressors: a focus on wildfire smoke and air quality

Scieszka,

Bolt,

McCormick

et al. 2023

Front. Toxicol.

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Aging is a complex biological process involving multiple interacting mechanisms and is being increasingly linked to environmental exposures such as wildfire smoke. In this review, we detail the hallmarks of aging, emphasizing the role of telomere attrition, cellular senescence, epigenetic alterations, proteostasis, genomic instability, and mitochondrial dysfunction, while also exploring integrative hallmarks - altered intercellular communication and stem cell exhaustion. Within each hallmark of aging, our review explores how environmental disasters like wildfires, and their resultant inhaled toxicants, interact with these aging mechanisms. The intersection between aging and environmental exposures, especially high-concentration insults from wildfires, remains under-studied. Preliminary evidence, from our group and others, suggests that inhaled wildfire smoke can accelerate markers of neurological aging and reduce learning capabilities. This is likely mediated by the augmentation of circulatory factors that compromise vascular and blood-brain barrier integrity, induce chronic neuroinflammation, and promote age-associated proteinopathy-related outcomes. Moreover, wildfire smoke may induce a reduced metabolic, senescent cellular phenotype. Future interventions could potentially leverage combined anti-inflammatory and NAD + boosting compounds to counter these effects. This review underscores the critical need to study the intricate interplay between environmental factors and the biological mechanisms of aging to pave the way for effective interventions.

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“…High COVID-19 morbidity and mortality in patients with diabetes, chronic obstructive pulmonary disease (COPD), or congestive heart failure (CHF) have been associated with increased counts of AMs in BALF (153). Increased AM counts in BALF have been also observed in patients with COPD, correlating with the disease severity (154), in mice following protracted exposure to diesel exhaust particles (155), in aged rodents (156), in mice subjected to heart failure following augmented hypertension (157), and in models of dilated cardiomyopathy combined with exercise (158). Furthermore, experimental aging and diabetic state was associated with altered distributions of AM phenotypes and their reduced bactericidal capacity (159)(160)(161).…”

Section: The Role Of Ams In Sars-cov-2-associated Ardsmentioning

confidence: 99%

The Role of Macrophages in the Pathogenesis of SARS-CoV-2-Associated Acute Respiratory Distress Syndrome

et al. 2021

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Macrophages are cells that mediate both innate and adaptive immunity reactions, playing a major role in both physiological and pathological processes. Systemic SARS-CoV-2-associated complications include acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation syndrome, edema, and pneumonia. These are predominantly effects of massive macrophage activation that collectively can be defined as macrophage activation syndrome. In this review we focus on the role of macrophages in COVID-19, as pathogenesis of the new coronavirus infection, especially in cases complicated by ARDS, largely depends on macrophage phenotypes and functionalities. We describe participation of monocytes, monocyte-derived and resident lung macrophages in SARS-CoV-2-associated ARDS and discuss possible utility of cell therapies for its treatment, notably the use of reprogrammed macrophages with stable pro- or anti-inflammatory phenotypes.

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Diesel exhaust exposure intensifies inflammatory and structural changes associated with lung aging in mice

Cited by 15 publications

References 36 publications

Dimethyl Fumarate Attenuates Lung Inflammation and Oxidative Stress Induced by Chronic Exposure to Diesel Exhaust Particles in Mice

Dimethyl Fumarate Attenuates Lung Inflammation and Oxidative Stress Induced by Chronic Exposure to Diesel Exhaust Particles in Mice

Aging, longevity, and the role of environmental stressors: a focus on wildfire smoke and air quality

The Role of Macrophages in the Pathogenesis of SARS-CoV-2-Associated Acute Respiratory Distress Syndrome

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