Search Results (15)

Background: As a well-known environmental hazard, ambient fine particulate matter (PM_2.5, aerodynamic diameter ≤ 2.5 µm) has been positively correlated with an increased risk of digestive system diseases, including appendicitis, inflammatory bowel disease, and gastrointestinal cancer. Additionally, PM_2.5 exposure has been shown to alter microbiota composition and diversity in human and animal models. However, its impact on goblet cells and gut mucus barrier integrity remains unclear. Methods: To address this, 8-week-old male and female interleukin-10 knockout (IL10^−/−) mice, serving as a spontaneous colitis model, were exposed to concentrated ambient PM_2.5 or filtered air (FA) in a whole-body exposure system for 17 weeks. Colon tissues from the PM_2.5-exposed mice and LS174T goblet cells were analyzed using H&E staining, transmission electron microscopy (TEM), and transcriptomic profiling. Results: The average PM_2.5 concentration in the exposure chamber was 100.20 ± 13.79 µg/m³. PM_2.5 exposure in the IL10^−/− mice led to pronounced colon shortening, increased inflammatory infiltration, ragged villi brush borders, dense goblet cells with sparse enterocytes, and lipid droplet accumulation in mitochondria. Similar ultrastructure changes were exhibited in the LS174T goblet cells after PM_2.5 exposure. Transcriptomic analysis revealed a predominantly upregulated gene expression spectrum, indicating an overall enhancement rather than suppression of metabolic activity after PM_2.5 exposure. Integrated enrichment analyses, including GO, KEGG, and GSEA, showed enrichment in pathways related to oxidative stress, xenobiotic (exogenous compound) metabolism, and energy metabolism. METAFlux, a metabolic activity analysis, further substantiated that PM_2.5 exposure induces a shift in cellular energy metabolism preference and disrupts redox homeostasis. Conclusions: The findings of exacerbated gut barrier impairment and goblet cell dysfunction following PM_2.5 exposure provide new evidence of environmental factors contributing to colitis, highlighting new perspectives on its role in the pathogenesis of colitis. Full article

This study evaluates the impact of PM2.5 exposure from wood combustion on reproductive health and fetal development using an experimental model in Sprague Dawley rats. The study was conducted in Temuco, Chile, where high levels of air pollution are primarily attributed to residential wood burning. A multigenerational exposure model was implemented using controlled exposure chambers with filtered (FA) and unfiltered (NFA) air. Second-generation (G2) female rats (n = 48) were exposed pregestationally (60 days) and gestationally (23 days) under four conditions: FA/FA, FA/NFA, NFA/FA, and NFA/NFA. PM2.5 concentration and composition were monitored using beta-ray attenuation and X-ray fluorescence spectrometry. Reproductive parameters, ovarian follicle counts, and hormonal levels were assessed via vaginal cytology, histological analysis, and chemiluminescence immunoassays. PM2.5 exposure disrupted estrous cyclicity (p = 0.0001), reduced antral and growing follicles (p = 0.0020; p = 0.0317), and increased post-implantation losses (p = 0.0149). Serum progesterone and estradiol levels were significantly altered (p < 0.05). Despite ovarian disruptions, fertility rates remained unchanged. These findings suggest that chronic exposure to wood smoke-derived PM2.5 adversely affects ovarian function and fetal growth without significantly impairing overall reproductive capacity. This study highlights the need for public health policies to mitigate wood smoke pollution. Full article

This study investigates the reactivity of municipal solid waste incineration residues to aqueous carbonation, focusing on CO₂ absorption rates, uptakes, and heavy metal (HM) leachability. Various combinations of boiler, electrofilter, and bag filter residues were assessed under typical incineration conditions. Bag filter residues from lime-sorbent plants exhibited the highest CO₂ uptake (244.5 gCO₂/kg), while bottom ash (BA) fine fraction, boiler/electrofilter fly ash (FA), and other mixed air pollution control residue (APCr) demonstrated uptakes of 101, 0, 93, and 167 gCO₂/kg, respectively. Carbonation kinetics revealed that high calcium content FA and APCr, followed similar CO₂ absorption trends. Notably, BA carbonation was predominantly driven by Ca-aluminates rather than lime. Carbonation reduces leaching of Al, As, Cd, Co, Cu, Ni, Pb and Zn compared to water washing, though significant concerns arise with anions such as Sb and Cr. In BA, critical behaviours of Cr, Mn, and Fe were observed, with Cr leaching likely controlled by Fe-Mn-Cr oxide particle dissolution. These findings highlight the potential of integrating enhanced metal recovery (EMR) through density or magnetic separation in BA prior to carbonation to reduce HM leaching and recycle critical metals (Ag, Cu, Cr, Ni, Mn, etc). Full article

Inflammatory bowel disease (IBD) is an immunologically complex disorder involving genetic, microbial, and environmental risk factors. Its global burden has continued to rise since industrialization, with epidemiological studies suggesting that ambient particulate matter (PM) in air pollution could be a contributing factor. Prior animal studies have shown that oral PM₁₀ exposure promotes intestinal inflammation in a genetic IBD model and that PM_2.5 inhalation exposure can increase intestinal levels of pro-inflammatory cytokines. PM₁₀ and PM_2.5 include ultrafine particles (UFP), which have an aerodynamic diameter of <0.10 μm and biophysical and biochemical properties that promote toxicity. UFP inhalation, however, has not been previously studied in the context of murine models of IBD. Here, we demonstrated that ambient PM is toxic to cultured Caco-2 intestinal epithelial cells and examined whether UFP inhalation affected acute colitis induced by dextran sodium sulfate and 2,4,6-trinitrobenzenesulfonic acid. C57BL/6J mice were exposed to filtered air (FA) or various types of ambient PM reaerosolized in the ultrafine size range at ~300 μg/m³, 6 h/day, 3–5 days/week, starting 7–10 days before disease induction. No differences in weight change, clinical disease activity, or histology were observed between the PM and FA-exposed groups. In conclusion, UFP inhalation exposure did not exacerbate intestinal inflammation in acute, chemically-induced colitis models. Full article

The coexistence of temperature changes and air pollution poses a severe global environmental issue, exacerbating health burdens. The aim of this study was to clarify the combined effects of ambient PM_2.5 and cold exposure on the development of metabolic disorders. Male C57BL/6 mice were randomly divided into four groups: T_N-FA, T_N-PM, T_C-FA and T_C-PM. The mice were then exposed to concentrated PM_2.5 or filtered air (FA) under normal (22 °C) or cold (4 °C) environment conditions for 4 weeks. Metabolic-disorder-related indicators, blood pressure, serous lipids, fasting blood glucose and insulin, energy metabolism, mitochondria and protein expression in tissues were detected for comprehensively assessing metabolic disorder. The results showed that, compared to being exposed to PM_2.5 only, when mice were exposed to both PM_2.5 and the cold (non-optimal), they exhibited more significant metabolic disorders regarding glucose tolerance (p < 0.05), insulin resistance (p < 0.05), lipid metabolism, adipocytes (p < 0.01) and mitochondrial function. This study suggested that a cold environment might substantially exacerbate PM_2.5-induced metabolic disorder. The interaction between temperature changes and air pollution implied that implementing the necessary environment-related policies is a critical and complex challenge. Full article

Lead (Pb) is a widespread heavy metal pollutant that interferes with plant growth. In this study, we investigated the effects of Pb on the mechanical and chemical properties of cell walls and on the growth of coleoptiles of rice (Oryza sativa L.) seedlings grown in the air (on moistened filter paper) and underwater (submerged condition). Coleoptile growth of air-grown seedlings was reduced by 40% by the 3 mM Pb treatment, while that of water-grown ones was reduced by 50% by the 0.5 mM Pb. Although the effective concentration of Pb for growth inhibition of air-grown coleoptiles was much higher than that of water-grown ones, Pb treatment significantly decreased the mechanical extensibility of the cell wall in air- and water-grown coleoptiles, when it inhibited their growth. Among the chemical components of coleoptile cell walls, the amounts of cell wall polysaccharides per unit fresh weight and unit length of coleoptile, which represent the thickness of the cell wall, were significantly increased in response to the Pb treatment (3 mM and 0.5 mM Pb for air- and water-grown seedlings, respectively), while the levels of cell wall-bound diferulic acids (DFAs) and ferulic acids (FAs) slightly decreased. These results indicate that Pb treatment increased the thickness of the cell wall but not the phenolic acid-mediated cross-linking structures within the cell wall in air- and water-grown coleoptiles. The Pb-induced cell wall thickening probably causes the mechanical stiffening of the cell wall and thus decreases cell wall extensibility. Such modifications of cell wall properties may be associated with the inhibition of coleoptile growth. The results of this study provide a new finding that Pb-induced cell wall remodeling contributes to the regulation of plant growth under Pb stress conditions via the modification of the mechanical property of the cell wall. Full article

Aerosols can contribute to plant nutrition via foliar uptake. The conditions for this are best at night because the humidity is high and hygroscopic, saline deposits can deliquesce as a result. Still, stomata tend to be closed at night to avoid unproductive water loss. However, if needed, nutrients are on the leaf surface, and plants could benefit from nocturnal stomatal opening because it further increases humidity in the leaf boundary layer and allows for stomatal nutrient uptake. We tested this hypothesis on P-deficient soil by comparing the influence of ambient aerosols and additional foliar P application on nocturnal transpiration. We measured various related leaf parameters, such as the foliar water loss, minimum leaf conductance (g_min), turgor loss point, carbon isotope ratio, contact angle, specific leaf area (SLA), tissue element concentration, and stomatal and cuticular characteristics. For untreated leaves grown in filtered, aerosol-free air (FA), nocturnal transpiration consistently decreased overnight, which was not observed for leaves grown in unfiltered ambient air (AA). Foliar application of a soluble P salt increased nocturnal transpiration for AA and FA leaves. Crusts on stomatal rims were shown by scanning electron microscopy, supporting the idea of stomatal uptake of deliquescent salts. Turgor loss point and leaf moisture content indicated a higher accumulation of solutes, due to foliar uptake by AA plants than FA plants. The hypothesis that deliquescent leaf surface salts may play a role in triggering nocturnal transpiration was supported by the results. Still, further experiments are required to characterize this phenomenon better. Full article

Exposure to ultrafine particles (UFPs, PM_0.1) during pregnancy triggers placental oxidative stress and inflammation, similar to fine PM (PM_2.5). The Nrf2 gene encodes a redox-sensitive transcription factor that is a major regulator of antioxidant and anti-inflammatory responses. Disruption of NRF2 is known to substantially enhance PM_2.5-driven oxidant and inflammatory responses; however, specific responses to UFP exposure, especially during critical windows of susceptibility such as pregnancy, are not fully characterized; To investigate the role of NRF2 in regulating maternal antioxidant defenses and placental responses to UFP exposure, wildtype (WT) and Nrf2^−/− pregnant mice were exposed to either low dose (LD, 100 µg/m³) or high dose (HD, 500 µg/m³) UFP mixture or filtered air (FA, control) throughout gestation; Nrf2^−/− HD-exposed female offspring exhibited significantly reduced fetal and placental weights. Placental morphology changes appeared most pronounced in Nrf2^−/− LD-exposed offspring of both sexes. Glutathione (GSH) redox analysis revealed significant increases in the GSH/GSSG ratio (reduced/oxidized) in WT female placental tissue exposed to HD in comparison with Nrf2^−/− HD-exposed mice. The expression of inflammatory cytokine genes (Il1β, Tnfα) was significantly increased in Nrf2^−/− placentas from male and female offspring across all exposure groups. Genes related to bile acid metabolism and transport were differentially altered in Nrf2^−/− mice across sex and exposure groups. Notably, the group with the most marked phenotypic effects (Nrf2^−/− HD-exposed females) corresponded to significantly higher placental Apoa1 and Apob expression suggesting a link between placental lipid transport and NRF2 in response to high dose UFP exposure; Disruption of NRF2 exacerbates adverse developmental outcomes in response to high dose UFP exposure in female offspring. Morphological effects in placenta from male and female offspring exposed to low dose UFPs also signify the importance of NRF2 in maternal–fetal response to UFPs. Full article

Early life exposure to particulate matter (PM) air pollution negatively impacts neonatal health. The underlying mechanisms following prenatal exposure, particularly to ultrafine particles (UFP, diameter ≤ 0.1 μm), are not fully understood; To evaluate the role of Nrf2 in response to in utero UFP exposure, we exposed time-mated Nrf2-deficient (Nrf2^−/−) or wildtype (WT) mice to filtered air (FA) or 100 μg/m³ ultrafine PM daily throughout pregnancy. Offspring were evaluated for pulmonary immunophenotypes and pulmonary/systemic oxidative stress on postnatal day 5, a timepoint at which we previously demonstrated viral respiratory infection susceptibility; Nrf2^−/− offspring exposed to FA had significantly lower average body weights compared to FA-exposed WT pups. Moreover, PM-exposed Nrf2^−/− offspring weighed significantly less than PM-exposed WT pups. Notably, PM-exposed Nrf2^−/− offspring showed a decreased pulmonary Th1/Th2 ratio, indicating a Th2 bias. Th17 cells were increased in FA-exposed Nrf2^−/− neonates yet decreased in PM-exposed Nrf2^−/− neonates. Analysis of oxidative stress-related genes in lung and oxidative stress biomarkers in liver tissues did not vary significantly across exposure groups or genotypes. Collectively, these findings indicate that the lack of Nrf2 causes growth inhibitory effects in general and in response to gestational UFP exposure. Prenatal UFP exposure skews CD4+ T lymphocyte differentiation toward Th2 in neonates lacking Nrf2, signifying its importance in maternal exposure and infant immune responses. Full article

Employing the optical redox imaging technique, we previously identified a significant redox shift of nicotinamide adenine dinucleotide (NAD and the reduced form NADH) in freshly isolated alveolar macrophages (AM) from ozone-exposed mice. The goal here was twofold: (a) to determine the NAD(H) redox shift in cryopreserved AM isolated from ozone-exposed mice and (b) to investigate whether there is a difference in the redox status between cryopreserved and freshly isolated AM. We found: (i) AM from ozone-exposed mice were in a more oxidized redox state compared to that from filtered air (FA)-exposed mice, consistent with the results obtained from freshly isolated mouse AM; (ii) under FA exposure, there was no significant NAD(H) redox difference between fresh AM that had been placed on ice for 2.5 h and cryopreserved AM; however, under ozone exposure, fresh AM were more oxidized than cryopreserved AM; (iii) via the use of nutrient starvation and replenishment and H₂O₂-induced oxidative stress of an AM cell line, we showed that this redox difference between cryopreserved and freshly isolated AM is likely the result of the double “hit”, i.e., the ozone-induced oxidative stress plus nutrient starvation that prevented freshly isolated AM from a full recovery after being on ice for a prolonged time period. The cryopreservation technique we developed eliminates/minimizes the effects of oxidative stress and nutrient starvation on cells. This method can be adopted to preserve lung macrophages from animal models or clinical patients for further investigations. Full article

Background: Human SP-A1 and SP-A2, encoded by SFTPA1 and SFTPA2, and their genetic variants differentially impact alveolar macrophage (AM) functions and regulation, including the miRNome. We investigated whether miRNome differences previously observed between AM from SP-A2 and SP-A1/SP-A2 mice are due to continued qualitative differences or a delayed response of mice carrying a single gene. Methods: Human transgenic (hTG) mice, carrying SP-A2 or both SP-A genes, and SP-A-KO mice were exposed to filtered air (FA) or ozone (O₃)_. AM miRNA levels, target gene expression, and pathways determined 18 h after O₃ exposure. RESULTS: We found (a) differences in miRNome due to sex, SP-A genotype, and exposure; (b) miRNome of both sexes was largely downregulated by O₃, and co-ex had fewer changed (≥2-fold) miRNAs than either group; (c) the number and direction of the expression of genes with significant changes in males and females in co-ex are almost the opposite of those in SP-A2; (d) the same pathways were found in the studied groups; and (e) O₃ exposure attenuated sex differences with a higher number of genotype-dependent and genotype-independent miRNAs common in both sexes after O₃ exposure. Conclusion: Qualitative differences between SP-A2 and co-ex persist 18 h post-O₃, and O₃ attenuates sex differences. Full article

Innate immune molecules, SP-A1 (6A², 6A⁴) and SP-A2 (1A⁰, 1A³), differentially affect young mouse survival after infection. Here, we investigated the impact of SP-A variants on the survival of aged mice. hTG mice carried a different SP-A1 or SP-A2 variant and SP-A-KO were either infected with Klebsiella pneumoniae or exposed to filtered air (FA) or ozone (O₃) prior to infection, and their survival monitored over 14 days. In response to infection alone, no gene- or sex-specific (except for 6A²) differences were observed; variant-specific survival was observed (1A⁰ > 6A⁴). In response to O₃, gene-, sex-, and variant-specific survival was observed with SP-A2 variants showing better survival in males than females, and 1A⁰ females > 1A³ females. A serendipitous, and perhaps clinically important observation was made; mice exposed to FA prior to infection exhibited significantly better survival than infected alone mice. 1A⁰ provided an overall better survival in males and/or females indicating a differential role for SP-A genetics. Improved ventilation, as provided by FA, resulted in a survival of significant magnitude in aged mice and perhaps to a lesser extent in young mice. This may have clinical application especially within the context of the current pandemic. Full article

Animal and epidemiological studies have suggested that exposure to airborne particulate matter (PM) with an aerodynamic diameter less than 2.5 μm (PM_2.5) is associated with the risk of developing type 2 diabetes. However, the mechanism underlying this risk is poorly understood. In the present study, we investigated the effects of PM_2.5 exposure on glucose homeostasis and related signaling pathways in mice. Wild-type and nuclear factor erythroid 2-related factor 2 (Nrf2) knockout (Nrf2^−/−) C57BL/6 male mice were exposed to either ambient concentrated PM_2.5 or filtered air (FA) for 12 weeks through a whole-body PM exposure system. At the end of the exposure, we assessed liver damage, and performed metabolic studies, gene expressions, as well as molecular signal transductions to determine the signaling pathways involving oxidative responses, insulin signaling, and glucose metabolism. Our results indicated that PM_2.5 exposure for 12 weeks caused significant liver damage as evidenced by elevated levels of aminotransferase (AST) and alanine aminotransferase (ALT). Furthermore, PM_2.5 exposure induced impaired glucose tolerance and inhibited glycogen synthesis, leading to hepatic insulin resistance indicated by higher glucose levels, higher area under the curve (AUC), and homeostasis model assessment of insulin resistance (HOMA-IR) values. We further found that PM_2.5 exposure significantly increased the expressions of Nrf2 and Nrf2-regulated antioxidant genes. Moreover, PM_2.5 exposure activated the c-Jun N-terminal kinase (JNK) signaling pathway and increased insulin receptor substrate-1 (IRS-1) phosphorylation at Ser³⁰⁷, but reduced protein kinase B phosphorylation at Ser⁴⁷³. Taken together, our study demonstrated PM_2.5 exposure triggered Nrf2-mediated oxidative responses and activated the JNK-mediated inhibitory signaling pathway, resulting in hepatic insulin resistance. Full article

Background: We have previously reported that in utero and early life exposure to diesel exhaust particulates predisposes mice to adult heart failure, and that in utero exposure alone is sufficient to confer this predisposition. This follow up study addresses whether neonatal exposure alone can also confer this predisposition. Methods: Newborn male C57BL/6 mice were exposed to diesel exhaust (DE) particulates immediately after birth until weaning at 21 days of age, whereupon they were transferred to filtered air (FA) conditions. At the age of 12 weeks, transverse aortic constriction (TAC) was performed followed by weekly echocardiography for three weeks. After the last echocardiogram, mice were euthanized for organ harvest, gravimetry and histology. Results: Neonatal exposure to DE particulates did not increase susceptibility to cardiac hypertrophy or heart failure after TAC when compared to FA exposed controls (ventricular weight/body weight ratio 7.505 vs. 7.517 mg/g, p = Not Significant (NS)). The left ventricular ejection fraction after TAC was similar between groups at one week, two weeks, and three weeks after procedure. Histological analysis showed no difference in the degree of cardiac hypertrophy or fibrosis. Conclusions: Neonatal exposure to DE particulates does not predispose mice to TAC-induced cardiac hypertrophy and heart failure in adulthood, in contrast to previously published results showing susceptibility due to in utero exposure. Full article

Studies suggest childhood exposure to environmental tobacco smoke (ETS) leads to increased incidence of infections of the lower respiratory tract. The objective of this study was to determine whether perinatal exposure to ETS increases the incidence, morbidity and severity of respiratory influenza infection and whether a secondary bacterial challenge at the peak of a pre-existing viral infection creates an enhanced host-pathogen susceptibility to an opportunistic infection. Timed-pregnant female Balb/c mice were exposed to either ETS for 6 h/day, 7 d/week beginning on gestation day 14 and continuing with the neonates to 6 weeks of age. Control animals were exposed to filtered air (FA). At the end of exposure, mice were intranasally inoculated with a murine-adapted influenza A. One week later, an intranasal inoculation of S. aureus bacteria was administered. The respective treatment groups were: bacteria only, virus only or virus+bacteria for both FA and ETS-exposed animals for a total of six treatment groups. Animal behavior and body weights were documented daily following infection. Mice were necropsied 1-day post-bacterial infection. Bronchoalveolar lavage fluid (BALF) cell analysis demonstrated perinatal exposure to ETS, compared to FA, leads to delayed but enhanced clinical symptoms and enhanced total cell influx into the lungs associated with viral infection followed by bacterial challenge. Viral infection significantly increases the number of neutrophils entering the lungs following bacterial challenge with either FA or ETS exposure, while the influx of lymphocytes and monocytes is significantly enhanced only by perinatal ETS exposure. There is a significant increase in peribronchiolar inflammation following viral infection in pups exposed to ETS compared with pups exposed to FA, but no change is noted in the degree of lung injury between FA and ETS-exposed animals following bacterial challenge. The data suggests perinatal exposure to ETS alters the response of neonates to the timing and severity of infection as well as ETS alters the pattern of inflammation and cellular influx into the lungs due to viral and bacterial infection. Full article