Exposure to fine particulate matter induces self-recovery and susceptibility of oxidative stress and inflammation in rat lungs

Ren, Haiwei; Lu, Jianjiang; Ning, Jianying; Su, Xianghui; Tong, Yanbin; Chen, Jiadeng; Ding, Yanzhou

doi:10.1007/s11356-020-10029-2

Cited by 21 publications

(9 citation statements)

References 52 publications

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“…Reactive oxygen species (ROS) have been reported to be an essential driving factor in the PM-mediated inflammatory response observed within the lungs [5]. PM 2.5 exposure is also well documented to induce pulmonary inflammation, often characterized by the expression of several inflammatory markers, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-10 [6,7]. Ambient air pollution PM has also been shown to induce Tolllike receptor 2 (TLR2) expression and subsequent activation of the nuclear factor kappa B (NF-κB) transcription factor that accelerates the inflammatory response in both in vitro studies and in vivo exposures [8].…”

Section: Introductionmentioning

confidence: 99%

Exposure to diesel exhaust particles results in altered lung microbial profiles, associated with increased reactive oxygen species/reactive nitrogen species and inflammation, in C57Bl/6 wildtype mice on a high-fat diet

et al. 2021

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Background Exposure to traffic-generated emissions is associated with the development and exacerbation of inflammatory lung disorders such as chronic obstructive pulmonary disorder (COPD) and idiopathic pulmonary fibrosis (IPF). Although many lung diseases show an expansion of Proteobacteria, the role of traffic-generated particulate matter pollutants on the lung microbiota has not been well-characterized. Thus, we investigated the hypothesis that exposure to diesel exhaust particles (DEP) can alter commensal lung microbiota, thereby promoting alterations in the lung’s immune and inflammatory responses. We aimed to understand whether diet might also contribute to the alteration of the commensal lung microbiome, either alone or related to exposure. To do this, we used male C57Bl/6 mice (4–6-week-old) on either regular chow (LF) or high-fat (HF) diet (45% kcal fat), randomly assigned to be exposed via oropharyngeal aspiration to 35 μg DEP, suspended in 35 μl 0.9% sterile saline or sterile saline only (control) twice a week for 30 days. A separate group of study animals on the HF diet was concurrently treated with 0.3 g/day of Winclove Ecologic® Barrier probiotics in their drinking water throughout the study. Results Our results show that DEP-exposure increases lung tumor necrosis factor (TNF)-α, interleukin (IL)-10, Toll-like receptor (TLR)-2, TLR-4, and the nuclear factor kappa B (NF-κB) histologically and by RT-qPCR, as well as Immunoglobulin A (IgA) and Immunoglobulin G (IgG) in the bronchoalveolar lavage fluid (BALF), as quantified by ELISA. We also observed an increase in macrophage infiltration and peroxynitrite, a marker of reactive oxygen species (ROS) + reactive nitrogen species (RNS), immunofluorescence staining in the lungs of DEP-exposed and HF-diet animals, which was further exacerbated by concurrent DEP-exposure and HF-diet consumption. Histological examinations revealed enhanced inflammation and collagen deposition in the lungs DEP-exposed mice, regardless of diet. We observed an expansion of Proteobacteria, by qPCR of bacterial 16S rRNA, in the BALF of DEP-exposed mice on the HF diet, which was diminished with probiotic-treatment. Conclusions Our findings suggest that exposure to DEP causes persistent and sustained inflammation and bacterial alterations in a ROS-RNS mediated fashion, which is exacerbated by concurrent consumption of an HF diet.

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Section: Introductionmentioning

confidence: 99%

Exposure to diesel exhaust particles results in altered lung microbial profiles, associated with increased reactive oxygen species/reactive nitrogen species and inflammation, in C57Bl/6 wildtype mice on a high-fat diet

et al. 2021

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“…Ji et al (2019), in a study of the effects and subsequent recovery at the end of PM 2.5 exposure, found that inflammatory cytokines and chemokines were persistently elevated in mice after 4 weeks of PM 2.5 exposure, but these effects all returned to normal levels within 2 weeks after cessation of exposure. A study by Ren et al (2020) also confirmed that PM 2.5 -induced damage to the organism could repair itself after cessation of exposure, but their further study found that this type of repair could not be considered a true repair. This is because significant changes were observed between groups when re-exposed to the same dose of PM 2.5 , which instead increased the susceptibility of target organs.…”

Section: Self-repair After Brain Injurymentioning

confidence: 98%

A review of respirable fine particulate matter (PM2.5)-induced brain damage

Lin

Xiao

et al. 2022

Front. Mol. Neurosci.

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Respirable fine particulate matter (PM2.5) has been one of the most widely publicized indicators of pollution in recent years. Epidemiological studies have established a strong association between PM2.5, lung disease, and cardiovascular disease. Recent studies have shown that PM2.5 is also strongly associated with brain damage, mainly cerebrovascular damage (stroke) and neurological damage to the brain (changes in cognitive function, dementia, psychiatric disorders, etc.). PM2.5 can pass through the lung–gas–blood barrier and the “gut–microbial–brain” axis to cause systemic oxidative stress and inflammation, or directly enter brain tissue via the olfactory nerve, eventually damaging the cerebral blood vessels and brain nerves. It is worth mentioning that there is a time window for PM2.5-induced brain damage to repair itself. However, the exact pathophysiological mechanisms of brain injury and brain repair are not yet fully understood. This article collects and discusses the mechanisms of PM2.5-induced brain injury and self-repair after injury, which may provide new ideas for the prevention and treatment of cerebrovascular and cerebral neurological diseases.

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“… 113 In COPD rats, PM2.5 increased malondialdehyde (MDA) levels while decreasing total superoxide dismutase (T-SOD). 114 Besides, in the lungs of COPD rats exposed to PM2.5, there was a decreasing trend in the expression of the Nrf2 protein and its downstream component heme oxygenase-1 (HO-1). 115 The transcription factor Nrf2, which is inversely correlated with the severity of COPD, controls the majority of antioxidants.…”

Section: Pm25 Induced Pathogenesis In Copdmentioning

confidence: 99%

The Effects and Pathogenesis of PM2.5 and Its Components on Chronic Obstructive Pulmonary Disease

Wang¹,

Li²

2023

COPD

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Chronic obstructive pulmonary disease (COPD), a heterogeneous disease, is the leading cause of death worldwide. In recent years, air pollution, especially particulate matter (PM), has been widely studied as a contributing factor to COPD. As an essential component of PM, PM2.5 is associated with COPD prevalence, morbidity, and acute exacerbations. However, the specific pathogenic mechanisms were still unclear and deserve further research. The diversity and complexity of PM2.5 components make it challenging to get its accurate effects and mechanisms for COPD. It has been determined that the most toxic PM2.5 components are metals, polycyclic aromatic hydrocarbons (PAHs), carbonaceous particles (CPs), and other organic compounds. PM2.5-induced cytokine release and oxidative stress are the main mechanisms reported leading to COPD. Nonnegligibly, the microorganism in PM 2.5 may directly cause mononuclear inflammation or break the microorganism balance contributing to the development and exacerbation of COPD. This review focuses on the pathophysiology and consequences of PM2.5 and its components on COPD.

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Exposure to fine particulate matter induces self-recovery and susceptibility of oxidative stress and inflammation in rat lungs

Cited by 21 publications

References 52 publications

Exposure to diesel exhaust particles results in altered lung microbial profiles, associated with increased reactive oxygen species/reactive nitrogen species and inflammation, in C57Bl/6 wildtype mice on a high-fat diet

Exposure to diesel exhaust particles results in altered lung microbial profiles, associated with increased reactive oxygen species/reactive nitrogen species and inflammation, in C57Bl/6 wildtype mice on a high-fat diet

A review of respirable fine particulate matter (PM2.5)-induced brain damage

The Effects and Pathogenesis of PM2.5 and Its Components on Chronic Obstructive Pulmonary Disease

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