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Influence of fine particulate matter and its pure particulate fractions on pulmonary immune cells and cytokines in mice.

ABSTRACT: Particulate matter with a diameter ≤2.5 µm (PM^2.5) has a complex composition and has been associated with the incidence of cardiopulmonary disease and premature death in humans. However, whether pure particulate fractions of PM^2.5 (PPP^2.5), which are composed primarily of carbon, are responsible for the toxicity caused by ambient particulate matter (original PM^2.5 particles, OPP^2.5) is currently unclear. The present study assessed the acute toxic effects of OPP^2.5 sampled in Beijing, China and of its PPP^2.5 fraction in male BALB/c mice. The mice were intratracheally instilled with a single dose of aerosolized OPP^2.5 or PPP^2.5. Blood, lungs and bronchoalveolar lavage fluid were collected after 24 h for histopathology, flow cytometry and the measurement of pro-inflammatory cytokines/chemokines and other biochemical factors. Both OPP^2.5 and PPP^2.5 caused acute toxicity, particularly inflammatory responses, including an increase in the levels of pro-inflammatory cytokines and an accumulation of numerous immune cells in the lungs. OPP^2.5 induced a stronger inflammatory response than PPP^2.5. The complex components adsorbed into the solid core granules of OPP^2.5 and the granules themselves contributed to the toxic effects.

SUBMITTER: Jiao Z

PROVIDER: S-EPMC8097186 | biostudies-literature | 2021 Jun

REPOSITORIES: biostudies-literature

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Influence of fine particulate matter and its pure particulate fractions on pulmonary immune cells and cytokines in mice.

Jiao Zhouguang Z Wen Zhanbo Z Yang Wenhui W Hu Lingfei L Li Jinsong J

Experimental and therapeutic medicine 20210421 6

Particulate matter with a diameter ≤2.5 µm (PM2.5) has a complex composition and has been associated with the incidence of cardiopulmonary disease and premature death in humans. However, whether pure particulate fractions of PM2.5 (PPP2.5), which are composed primarily of carbon, are responsible for the toxicity caused by ambient particulate matter (original PM2.5 particles, OPP2.5) is currently unclear. The present study assessed the acute ...[more]

PMID: 33968192

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Project description:Fine particulate matter (PM2.5) released during the livestock industry endangers the respiratory health of animals. Our previous findings suggested that broilers exposed to PM2.5 exhibited lung inflammation and changes in the pulmonary microbiome. Therefore, this study was to investigate whether the pulmonary microbiota plays a causal role in the pathogenesis of PM2.5-induced lung inflammation. We first used antibiotics to establish a pulmonary microbiota intervention broiler model, which showed a significantly reduced total bacterial load in the lungs without affecting the microbiota composition or structure. Based on it, 45 AA broilers of similar body weight were randomly assigned to three groups: control (CON), PM2.5 (PM), and pulmonary microbiota intervention (ABX-PM). From 21 d of age, broilers in the ABX-PM group were intratracheally instilled with antibiotics once a day for 3 d. Meanwhile, broilers in the other two groups were simultaneously instilled with sterile saline. On 24 and 26 d of age, broilers in the PM and ABX-PM groups were intratracheally instilled with PM2.5 suspension to induce lung inflammation, and broilers in the CON group were simultaneously instilled with sterile saline. The lung histomorphology, inflammatory cytokines' expression levels, lung microbiome, and microbial growth conditions were analyzed to determine the effect of the pulmonary microbiota on PM2.5-induced lung inflammation. Broilers in the PM group showed lung histological injury, while broilers in the ABX-PM group had normal lung histomorphology. Furthermore, microbiota intervention significantly reduced mRNA expression levels of interleukin-1β, tumor necrosis factor-α, interleukin-6, interleukin-8, toll-like receptor 4 and nuclear factor kappa-B. PM2.5 induced significant changes in the β diversity and structure of the pulmonary microbiota in the PM group. However, no significant changes in microbiota structure were observed in the ABX-PM group. Moreover, the relative abundance of Enterococcus cecorum in the PM group was significantly higher than that in the CON and ABX-PM groups. And sterile bronchoalveolar lavage fluid from the PM group significantly promoted the growth of E. cecorum, indicating that PM2.5 altered the microbiota's growth condition. In conclusion, pulmonary microbiota can affect PM2.5-induced lung inflammation in broilers. PM2.5 can alter the bacterial growth environment and promote dysbiosis, potentially exacerbating inflammation.

Project description:BackgroundAir pollution, especially fine particulate matter (PM), can cause brain damage, cognitive decline, and an increased risk of neurodegenerative disease, especially alzheimer's disease (AD). Typical pathological findings of amyloid and tau protein accumulation have been detected in the brain after exposure in animal studies. However, these observations were based on high levels of PM exposure, which were far from the WHO guidelines and those present in our environment. In addition, white matter involvement by air pollution has been less reported. Thus, this experiment was designed to simulate the true human world and to discuss the possible white matter pathology caused by air pollution.Results6 month-old female 3xTg-AD mice were divided into exposure and control groups and housed in the Taipei Air Pollutant Exposure System (TAPES) for 5 months. The mice were subjected to the Morris water maze test after exposure and were then sacrificed with brain dissection for further analyses. The mean mass concentration of PM2.5 during the exposure period was 13.85 μg/m3. After exposure, there was no difference in spatial learning function between the two groups, but there was significant decay of memory in the exposure group. Significantly decreased total brain volume and more neuronal death in the cerebral and entorhinal cortex and demyelination of the corpus callosum were noted by histopathological staining after exposure. However, there was no difference in the accumulation of amyloid or tau on immunohistochemistry staining. For the protein analysis, amyloid was detected at significantly higher levels in the cerebral cortex, with lower expression of myelin basic protein in the white matter. A diffuse tensor image study also revealed insults in multiple white matter tracts, including the optic tract.ConclusionsIn conclusion, this pilot study showed that even chronic exposure to low PM2.5 concentrations still caused brain damage, such as gross brain atrophy, cortical neuron damage, and multiple white matter tract damage. Typical amyloid cascade pathology did not appear prominently in the vulnerable brain region after exposure. These findings imply that multiple pathogenic pathways induce brain injury by air pollution, and the optic nerve may be another direct invasion route in addition to olfactory nerve.

Dataset Information

Influence of fine particulate matter and its pure particulate fractions on pulmonary immune cells and cytokines in mice.

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Influence of fine particulate matter and its pure particulate fractions on pulmonary immune cells and cytokines in mice.

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