Role of Estrogen on Alveolar Macrophage Polarization in Response to Particulate Matter Exposure

Particulate matter (PM) exposure is linked to the worsening of respiratory conditions, including allergic rhinitis (AR), as it can trigger nasal and systemic inflammation. To unveil the underlying molecular mechanisms, we investigated the effects of PM exposure on the release of plasmatic extracellular vesicles (EV) and on the complex cross-talk between the host and the nasal microbiome. To this aim, we evaluated the effects of PM10 and PM2.5 exposures on both the bacteria-derived-EV portion (bEV) and the host-derived EVs (hEV), as well as on bacterial nasal microbiome (bNM) features in 26 AR patients and 24 matched healthy subjects (HS). In addition, we assessed the role exerted by the bNM as a modifier of PM effects on the complex EV signaling network in the paradigmatic context of AR. We observed that PM exposure differently affected EV release and bNM composition in HS compared to AR, thus potentially contributing to the molecular mechanisms underlying AR. The obtained results represent the first step towards the understanding of the complex signaling network linking external stimuli, bNM composition, and the immune risponse.

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Role of Tilianin against Acute Lung Injury in In Vitro LPS-Induced Alveolar Macrophage Cells and an In Vivo C57BL/6 Mice Model

Journal of Environmental Pathology Toxicology and Oncology ◽

10.1615/jenvironpatholtoxicoloncol.2020035136 ◽

2020 ◽

Vol 39 (4) ◽

pp. 335-344

Author(s):

Yonghong Zhang ◽

Zhenshuai Fu

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Alveolar Macrophage ◽

Mice Model ◽

Macrophage Cells

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The short-term effects of particulate matter exposure on asthma-related hospital visits in Korea: based on the national health insurance data

10.26226/morressier.5acc8acfd462b8028d89a637 ◽

2018 ◽

Author(s):

Dae Jin Song

Keyword(s):

Particulate Matter ◽

Health Insurance ◽

National Health Insurance ◽

National Health ◽

Short Term ◽

Health Insurance Data ◽

Hospital Visits ◽

Insurance Data ◽

Particulate Matter Exposure ◽

Short Term Effects

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Exercise Performed Concomitantly with Particulate Matter Exposure Inhibits Lung Injury

International Journal of Sports Medicine ◽

10.1055/s-0043-121147 ◽

2017 ◽

Vol 39 (02) ◽

pp. 133-140 ◽

Cited By ~ 2

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.

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Exosomes from human umbilical cord mesenchymal stem cells attenuate the inflammation of severe steroid-resistant asthma by reshaping macrophage polarization

Stem Cell Research & Therapy ◽

10.1186/s13287-021-02244-6 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Bing Dong ◽

Chao Wang ◽

Jing Zhang ◽

Jinrong Zhang ◽

Yinuo Gu ◽

...

Keyword(s):

Flow Cytometry ◽

Stem Cell ◽

Mesenchymal Stem Cell ◽

Quantitative Proteomics ◽

Macrophage Polarization ◽

Human Umbilical Cord ◽

Raw 264.7 ◽

Steroid Resistant ◽

Central Protein

Abstract Background Severe, steroid-resistant asthma (SSRA) is a serious clinical problem in asthma management. Affected patients have severe clinical symptoms, worsened quality of life, and do not respond to steroid, a mainstay steroid treatment of asthma. Thus, effective therapies are urgently needed. Exosomes derived from mesenchymal stem cell (MSC-Exo) has become attractive candidates for the lung inflammatory diseases through its immunomodulatory effects. In this study, we explored the therapeutic effects of MSC-Exo in SSRA and identified the therapeutic mechanism of MSC-Exo. Method Exosomes from human umbilical cord mesenchymal stem cell (hUCMSC) were isolated and characterized by transmission electron microscopy, nanoparticle tracking analysis and flow cytometry analysis. Effects of MSC-Exo on airway hyper responsiveness (AHR), inflammation, histopathology, and macrophage polarization in SSRA in mice were evaluated. Systematic depletion of macrophages determined the role of macrophages in the therapeutic effect of SSRA in mice. LPS-stimulated RAW 264.7 cell model was constructed to determine the underlying mechanism of MSC-Exo on macrophage polarization. qRT-PCR, Western blotting, immunofluorescence, and flow cytometry were performed to evaluate the expression of M1 or M2 markers. Tandem mass tags (TMT)-labeled quantitative proteomics were applied to explore the central protein during the regulation effect of MSC-Exo on macrophage polarization. Knockdown and overexpression of TRAF1 were used to further clarify the role of the central protein on macrophage polarization. Result We successfully isolated and characterized exosomes from hUCMSCs. We verified that the intratracheal administration of MSC-Exo reversed AHR, histopathology changes, and inflammation in SSRA mice. Systematic depletion of macrophages weakened the therapeutic effect of MSC-Exo. We found that MSC-Exo treatment inhibited M1 polarization and promoted M2 polarization in LPS-stimulated RAW 264.7 cells. Subsequently, tumor necrosis factor receptor-associated factor 1 (TRAF1) was determined as the central protein which may be closely related to the regulation of macrophage polarization from TMT-labeled quantitative proteomics analysis. Knockdown and overexpression of TRAF1 demonstrated that the effect of MSC-Exo treatment on macrophage polarization, NF-κB and PI3K/AKT signaling was dependent on TRAF1. Conclusion MSC-Exo can ameliorate SSRA by moderating inflammation, which is achieved by reshaping macrophage polarization via inhibition of TRAF1.

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