scholarly journals The Effect of Particulate Matter Exposure on the Inflammatory Airway Response of Street Runners and Sedentary People

Atmosphere ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 43 ◽  
Author(s):  
Lucas G. Pagani ◽  
Juliana M.B. Santos ◽  
Roberta Foster ◽  
Marcelo Rossi ◽  
Luiz A. Luna Junior ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Inflammatory Responses ◽  
Sedentary Lifestyle ◽  
Upper Airway ◽  
Polluted Environment ◽  
Fractional Exhaled Nitric Oxide ◽  
Upper Airways ◽  
Tnf Α ◽  
Airway Response ◽  
Particulate Matter Exposure

Physical exercise promotes many health benefits. However, its effects are not well known in a polluted environment. Thus, this study aimed to compare upper airway inflammatory responses between street runners and sedentary individuals. Twenty-eight volunteers were recruited: runners (n = 14) and sedentary individuals (n = 14), who lived and worked in the same metropolitan area of São Paulo, Brazil. Particulate matter (PM) levels were monitored ten weeks before winter (low PM levels) and ten weeks after the beginning of winter (high PM levels) [PM10 (p < 0.0001) and PM2.5 (p < 0.0001)]. The cytokines (TNF-α, IL-6, IL-10, and IL-17A) levels in the nasal lavage and fractional exhaled nitric oxide (FeNO) were taken at the beginning of the winter (baseline) and ten weeks afterwards (after ten weeks of high PM exposure). IL-6 concentration increased in both runners (p = 0.037) and sedentary individuals (p = 0.027) after high PM exposure compared to the baseline. IL-10 concentration increased in sedentary individuals (p = 0.037) while IL-17A levels were increased in runners (p = 0.001) after high PM exposure compared to the baseline. FeNO levels decreased in runners (p = 0.025) after high PM exposure compared to the baseline. Outdoor endurance training acts as an inducer of a differentiated immune response in the upper airways of runners compared to individuals with a sedentary lifestyle from the same community after elevated PM exposure.

Comparison of upper and lower airway responses of two sensitized rat strains to inhaled antigen

1992 ◽  
Vol 73 (4) ◽  
pp. 1608-1613 ◽  
Author(s):  
L. J. Xu ◽  
S. Sapienza ◽  
T. Du ◽  
S. Waserman ◽  
J. G. Martin
Keyword(s):  
Upper Airway ◽  
Brown Norway ◽  
Lower Airway ◽  
Sprague Dawley ◽  
Pulmonary Resistance ◽  
Upper Airways ◽  
Tracheal Pressure ◽  
Airway Response ◽  
Airway Responses ◽  
Inbred Rat

The purpose of the study was to investigate the relationships between upper airways responses and pulmonary responses of two strains of highly inbred rats to inhaled antigen. To do this we measured the upper and lower airways resistance for 60 min after challenge of Brown-Norway rats (BN; n = 13) and an inbred rat strain (MF; n = 11), derived from Sprague-Dawley, with aerosolized ovalbumin (OA). Rats were actively sensitized with OA (1 mg sc) using Bordetella pertussis as an adjuvant. Two weeks later the animals were anesthetized and challenged. Tracheal pressure, esophageal pressure, and airflow were measured, from which total pulmonary resistance was partitioned into upper airway and lower pulmonary resistance (RL). The peak upper airway response to inhaled OA was similar in BN (1.89 +/- 0.66 cmH2O.ml-1.s; n = 7) and MF (2.85 +/- 0.68 cmH2O.ml-1.s; n = 6). The lower airway response to OA challenge was substantially greater in BN, and RL changed from 0.07 +/- 0.01 to 0.34 +/- 0.13 (n = 6; P < 0.05). The MF did not have any significant increase in RL after challenge; the baseline RL was 0.12 +/- 0.02 and only reached a peak value of 0.15 +/- 0.05 (n = 5; P = NS). Lower airway responsiveness of BN (n = 10) to serotonin, an important mediator early allergic airway responses, was similar to MF (n = 7).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Outdoor Endurance Training with Air Pollutant Exposure Versus Sedentary Lifestyle: A Comparison of Airway Immune Responses

2019 ◽  
Vol 16 (22) ◽  
pp. 4418 ◽  
Author(s):  
Juliana de Melo Batista dos Santos ◽  
Roberta Foster ◽  
Anne-Charlotte Jonckheere ◽  
Marcelo Rossi ◽  
Luiz Antonio Luna Junior ◽  
...  
Keyword(s):  
Immune Response ◽  
Endurance Training ◽  
Inflammatory Responses ◽  
Sedentary Lifestyle ◽  
Air Pollutant ◽  
Cell Protein ◽  
Response Analysis ◽  
Inflammatory Status ◽  
Tnf Α ◽  
Ifn Γ

Although regular exercise-training improves immune/inflammatory status, the influence of air pollutants exposure during outdoor endurance training compared to a sedentary lifestyle has not yet been clarified. This study aimed to compare the immune/inflammatory responses in the airways of street runners and sedentary people after acute and chronic particulate matter (PM) exposure. Forty volunteers (street runners (RUN, n = 20); sedentary people (SED, n = 20)) were evaluated 1 (acute) and 10 (chronic) weeks after PM exposure. Cytokines [interferon (IFN)-γ, tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-10, IL-13, and IL-17A] in nasal lavage fluid, salivary antibacterial peptides (lactoferrin (LTF), cathelicidin (LL-37), defensin-α 1–3), and secretory immunoglobulin A (SIgA), plasma club cell protein (CC16), and fractional exhaled nitric oxide (FeNO) were analyzed. After acute exposure, the RUN group showed lower levels of IL-13, IL-10, and FeNO, but higher defensin-α than the SED group. After chronic exposure, the RUN group showed elevation of IFN-γ, IL-10, IL-17A, and a decrease of FeNO levels, whereas the SED group showed elevation of TNF-α, IL-6, IL-10, and a decrease of IL-13 levels. Comparing these groups, the RUN group showed higher levels of SIgA and LTF, and lower FeNO levels than the SED group. In relation to the Th immune response analysis after acute and chronic PM exposure, the RUN group showed a pattern associated with Th1, while in the SED group, a Th2 pattern was found. Both groups showed also a Th17 immune response pattern. Our results allow us to suggest that the immune/inflammatory status of the respiratory tract after acute and chronic PM exposure was improved by the long-standing regular practice of outdoor endurance exercise compared to a sedentary lifestyle.

scholarly journals Chemical and Biological Characterization of Particulate Matter (PM 2.5) and Volatile Organic Compounds Collected at Different Sites in the Los Angeles Basin

2020 ◽  
Vol 10 (9) ◽  
pp. 3245
Author(s):  
Arthur K. Cho ◽  
Yasuhiro Shinkai ◽  
Debra A. Schmitz ◽  
Emma Di Stefano ◽  
Arantza Eiguren-Fernandez ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Volatile Organic Compounds ◽  
Los Angeles ◽  
Organic Compounds ◽  
Inflammatory Responses ◽  
Biological Properties ◽  
Heme Oxygenase 1 ◽  
Tnf Α ◽  
Volatile Organic

Background: Most studies on air pollution (AP) exposure have focused on adverse health effects of particulate matter (PM). Less well-studied are the actions of volatile organic compounds (VOCs) not retained in PM collections. These studies quantified chemical and biological properties of both PM2.5 and VOCs. Methods: Samples were collected near the Port of Los Angeles (Long Beach, LB), railroads (Commerce, CM), and a pollution-trapping topography-site (San Bernardino, SB). Quantitative assays were conducted: (1) chemical—prooxidant and electrophile content, (2) biological—tumor necrosis factor-α (TNF-α) and heme oxygenase-1 (HO-1) expression (3), VOC modulation of PM effects and (4), activation of the antioxidant response element (ARE) using murine RAW 264.7 macrophages. Results: SB site samples were the most potent in the chemical and biological assays, followed by a CM railroad site. Only PM2.5 exhibited significant proinflammatory responses. VOCs were more potent than PM2.5 in generating anti-inflammatory responses; further, VOC pretreatment reduced PM-associated TNF-α expression. VOCs significantly increased ARE activation compared to their corresponding PM2.5 which remained at background levels. Conclusion: Ambient VOCs are major contributors to adaptive responses that can modulate PM effects, in vitro, and, as such, need to be included in comprehensive assessments of AP.

Particulate Matter Exposure Exacerbates Amyloid-β Plaque Deposition and Gliosis in APP/PS1 Mice

2021 ◽  
Author(s):  
Bijayani Sahu ◽  
Amy R. Mackos ◽  
Angela M. Floden ◽  
Loren E. Wold ◽  
Colin K. Combs
Keyword(s):  
Air Pollution ◽  
Particulate Matter ◽  
Molecular Mechanisms ◽  
Neurodegenerative Disorder ◽  
Amyloid Β ◽  
Plaque Deposition ◽  
Tnf Α ◽  
Plaque Load ◽  
Genetic And Environmental Factors ◽  
Particulate Matter Exposure

Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of amyloid-β (Aβ) plaques, neuroinflammation, and neuronal death. There are several well-established genetic and environmental factors hypothesized to contribute to AD progression including air pollution. However, the molecular mechanisms by which air pollution exacerbates AD are unclear. Objective: This study explored the effects of particulate matter exposure on AD-related brain changes using the APP/PS1 transgenic model of disease. Methods: Male C57BL/6;C3H wild type and APP/PS1 mice were exposed to either filtered air (FA) or particulate matter sized under 2.5 μm (PM2.5) for 6 h/day, 5 days/week for 3 months and brains were collected. Immunohistochemistry for Aβ, GFAP, Iba1, and CD68 and western blot analysis for PS1, BACE, APP, GFAP, and Iba1 were performed. Aβ ELISAs and cytokine arrays were performed on frozen hippocampal and cortical lysates, respectively. Results: The Aβ plaque load was significantly increased in the hippocampus of PM2.5-exposed APP/PS1 mice compared to their respective FA controls. Additionally, in the PM2.5-exposed APP/PS1 group, increased astrocytosis and microgliosis were observed as indicated by elevated GFAP, Iba1, and CD68 immunoreactivities. PM2.5 exposure also led to an elevation in the levels of PS1 and BACE in APP/PS1 mice. The cytokines TNF-α, IL-6, IL-1β, IFN-γ, and MIP-3α were also elevated in the cortices of PM2.5-exposed APP/PS1 mice compared to FA controls. Conclusion: Our data suggest that chronic particulate matter exposure exacerbates AD by increasing Aβ plaque load, gliosis, and the brain inflammatory status.

Anti-β2 Glycoprotein I Antibodies Cause Inflammation and Recruit Dendritic Cells in Platelet Clearance

2001 ◽  
Vol 86 (11) ◽  
pp. 1257-1263 ◽  
Author(s):  
Attilio Bondanza ◽  
Angelo Manfredi ◽  
Valérie Zimmermann ◽  
Matteo Iannacone ◽  
Angela Tincani ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Inflammatory Responses ◽  
Glycoprotein I ◽  
Activated Platelets ◽  
Tnf Α ◽  
Per Se ◽  
Antigen Presenting ◽  
Antiinflammatory Cytokine

SummaryScavenger phagocytes are mostly responsible for the in vivo clearance of activated or senescent platelets. In contrast to other particulate substrates, the phagocytosis of platelets does not incite pro-inflammatory responses in vivo. This study assessed the contribution of macrophages and dendritic cells (DCs) to the clearance of activated platelets. Furthermore, we verified whether antibodies against the β2 Glycoprotein I (β2GPI), which bind to activated platelets, influence the phenomenon. DCs did not per se internalise activated platelets. In contrast, macrophages efficiently phagocytosed platelets. In agreement with the uneventful nature of the clearance of platelets in vivo, phagocytosing macrophages did not release IL-1β, TNF-α or IL-10. β2GPI bound to activated platelets and was required for their recognition by anti-ββ2GPI antibodies. DCs internalised platelets opsonised by anti-ββ2GPI antibodies. The phagocytosis of opsonised platelets determined the release of TNF-α and IL-1β by DCs and macrophages. Phagocytosing macrophages, but not DCs, secreted the antiinflammatory cytokine IL-1β0. We conclude that anti-ββ2GPI antibodies cause inflammation during platelet clearance and shuttle platelet antigens to antigen presenting DCs.

scholarly journals Punicalagin Prevents Inflammation in LPS-Induced RAW264.7 Macrophages by Inhibiting FoxO3a/Autophagy Signaling Pathway

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2794 ◽  
Author(s):  
Cao ◽  
Chen ◽  
Ren ◽  
Zhang ◽  
Tan ◽  
...  
Keyword(s):  
Western Blot ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Inflammatory Responses ◽  
Raw264.7 Macrophages ◽  
Tnf Α ◽  
Autophagy Inhibition ◽  
Pro Inflammatory Cytokines

Punicalagin, a hydrolysable tannin of pomegranate juice, exhibits multiple biological effects, including inhibiting production of pro-inflammatory cytokines in macrophages. Autophagy, an intracellular self-digestion process, has been recently shown to regulate inflammatory responses. In this study, we investigated the anti-inflammatory potential of punicalagin in lipopolysaccharide (LPS) induced RAW264.7 macrophages and uncovered the underlying mechanisms. Punicalagin significantly attenuated, in a concentration-dependent manner, LPS-induced release of NO and decreased pro-inflammatory cytokines TNF-α and IL-6 release at the highest concentration. We found that punicalagin inhibited NF-κB and MAPK activation in LPS-induced RAW264.7 macrophages. Western blot analysis revealed that punicalagin pre-treatment enhanced LC3II, p62 expression, and decreased Beclin1 expression in LPS-induced macrophages. MDC assays were used to determine the autophagic process and the results worked in concert with Western blot analysis. In addition, our observations indicated that LPS-induced releases of NO, TNF-α, and IL-6 were attenuated by treatment with autophagy inhibitor chloroquine, suggesting that autophagy inhibition participated in anti-inflammatory effect. We also found that punicalagin downregulated FoxO3a expression, resulting in autophagy inhibition. Overall these results suggested that punicalagin played an important role in the attenuation of LPS-induced inflammatory responses in RAW264.7 macrophages and that the mechanisms involved downregulation of the FoxO3a/autophagy signaling pathway.

Exercise Performed Concomitantly with Particulate Matter Exposure Inhibits Lung Injury

2017 ◽  
Vol 39 (02) ◽  
pp. 133-140 ◽  
Author(s):  
Adriano Silva-Renno ◽  
Guilherme Baldivia ◽  
Manoel Oliveira-Junior ◽  
Maysa Brandao-Rangel ◽  
Elias El-Mafarjeh ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Systemic Inflammation ◽  
Air Pollutants ◽  
Lung Parenchyma ◽  
Treadmill Training ◽  
Tnf Alpha ◽  
Systemic Response ◽  
Pm 2.5 ◽  
Pm 10 ◽  
Particulate Matter Exposure

AbstractAir pollution is a growing problem worldwide, inducing and exacerbating several diseases. Among the several components of air pollutants, particulate matter (PM), especially thick (10–2.5 µm; PM 10) and thin (≤2.5 µm; PM 2.5), are breathable particles that easily can be deposited within the lungs, resulting in pulmonary and systemic inflammation. Although physical activity is strongly recommended, its effects when practiced in polluted environments are questionable. Therefore, the present study evaluated the pulmonary and systemic response of concomitant treadmill training with PM 2.5 and PM 10 exposure. Treadmill training inhibited PM 2.5- and PM 10-induced accumulation of total leukocytes (p<0.001), neutrophils (p<0.001), macrophages (p<0.001) and lymphocytes (p<0.001) in bronchoalveolar lavage (BAL), as well as the BAL levels of IL-1beta (p<0.001), CXCL1/KC (p<0.001) and TNF-alpha (p<0.001), whereas it increased IL-10 levels (p<0.05). Similar effects were observed on accumulation of polymorphonuclear (p<0.01) and mononuclear (p<0.01) cells in the lung parenchyma and in the peribronchial space. Treadmill training also inhibited PM 2.5- and PM 10-induced systemic inflammation, as observed in the number of total leukocytes (p<0.001) and in the plasma levels of IL-1beta (p<0.001), CXCL1/KC (p<0.001) and TNF-alpha (p<0.001), whereas it increased IL-10 levels (p<0.001). Treadmill training inhibits lung and systemic inflammation induced by particulate matter.

Prenatal particulate matter exposure and Intrauterine Fetal Death

2021 ◽  
Vol 234 ◽  
pp. 113720
Author(s):  
Tamar Wainstock ◽  
Israel Yoles ◽  
Ruslan Sergienko ◽  
Itai Kloog ◽  
Eyal Sheiner
Keyword(s):  
Particulate Matter ◽  
Fetal Death ◽  
Intrauterine Fetal Death ◽  
Particulate Matter Exposure
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