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      Administration of Lactobacillus paracasei HB89 mitigates PM 2.5-induced enhancement of inflammation and allergic airway response in murine asthma model

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      Journal: PLoS ONE
      Publisher: Public Library of Science

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          Abstract

          PM 2.5 causes abnormal immune response and asthma in animals. In this study, a Balb/c mouse animal model was exposed to PM 2.5 to induce asthma. Lactobacillus paracasei HB89 was fed at the same time, in order to observe whether L. paracasei HB89 mitigates respiratory tract allergies stimulated by PM 2.5. The results showed that PM 2.5 stimulated a significant increase in white blood cells and immunoglobulin (IgE) in OVA-induced allergic Balb/c mice, and IgE in the blood further triggered the release of histamine in the lung immune cells. This not only increased overall immune cell counts, but the lymphocyte counts also increased significantly, resulting in significant inhibitions of cytokines INF-r and TGF-β, and induction of IL-4, IL-5, IL-13 and IL-17a. After feeding with HB89, apart from the absence of observable changes in body weight, the total white blood cell count in the animal blood and IgE response were also be reduced; the proliferation of immune cells in the lungs caused by PM 2.5 was slowed down; and histamine and cytokines INF-r and TGF-β were secreted in large quantities, but IL- 4, IL-5, IL-13, IL-17a were inhibited, which effectively reduced the possibility of asthma induction.

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          Most cited references29

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          Ambient Air Pollution and Pregnancy Outcomes: A Review of the Literature

          Radim J. Sram, Blanka Binkova, Jan Dejmek (posthumous) … (2005)
          Over the last decade or so, a large number of studies have investigated the possible adverse effects of ambient air pollution on birth outcomes. We reviewed these studies, which were identified by a systematic search of the main scientific databases. Virtually all reviewed studies were population based, with information on exposure to air pollution derived from routine monitoring sources. Overall, there is evidence implicating air pollution in adverse effects on different birth outcomes, but the strength of the evidence differs between outcomes. The evidence is sufficient to infer a causal relationship between particulate air pollution and respiratory deaths in the postneonatal period. For air pollution and birth weight the evidence suggests causality, but further studies are needed to confirm an effect and its size and to clarify the most vulnerable period of pregnancy and the role of different pollutants. For preterm births and intrauterine growth retardation (IUGR) the evidence as yet is insufficient to infer causality, but the available evidence justifies further studies. Molecular epidemiologic studies suggest possible biologic mechanisms for the effect on birth weight, premature birth, and IUGR and support the view that the relation between pollution and these birth outcomes is genuine. For birth defects, the evidence base so far is insufficient to draw conclusions. In terms of exposure to specific pollutants, particulates seem the most important for infant deaths, and the effect on IUGR seems linked to polycyclic aromatic hydrocarbons, but the existing evidence does not allow precise identification of the different pollutants or the timing of exposure that can result in adverse pregnancy outcomes.
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            Heart rate variability associated with particulate air pollution

            C.Arden Pope, Richard L Verrier, Eric G Lovett … (1999)
            Epidemiologic studies have linked fine particulate air pollution with cardiopulmonary mortality, yet underlying biologic mechanisms remain unknown. Changes in heart rate variability (HRV) may reflect changes in cardiac autonomic function and risk of sudden cardiac death. This study evaluated changes in mean heart rate and HRV in human beings associated with changes in exposure to particulate air pollution. Repeated ambulatory electrocardiographic monitoring was conducted on 7 subjects for a total of 29 person-days before, during, and after episodes of elevated pollution. Mean HR, the standard deviation of normal-to-normal (NN) intervals (SDNN), the standard deviation of the averages of NN intervals in all 5-minute segments of the recording (SDANN), and the square root of the mean of squared differences between adjacent NN intervals (r-MSSD) were calculated for 24-hour and 6-hour time segments. Associations of HRV with particulate pollution levels were evaluated with fixed-effects regression models. After controlling for differences across patients, elevated particulate levels were associated with (1) increased mean HR, (2) decreased SDNN, a measure of overall HRV, (3) decreased SDANN, a measure that corresponds to ultralow frequency variability, and (4) increased r-MSSD, a measure that corresponds to high-frequency variability. The associations between HRV and particulates were small but persisted even after controlling for mean HR. This study suggests that changes in cardiac autonomic function reflected by changes in mean HR and HRV may be part of the pathophysiologic mechanisms or pathways linking cardiovascular mortality and particulate air pollution.
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              Passage of inhaled particles into the blood circulation in humans.

              A Nemmar, P Hoet, B Vanquickenborne … (2002)
              Pollution by particulates has been consistently associated with increased cardiovascular morbidity and mortality. However, the mechanisms responsible for these effects are not well-elucidated. To assess to what extent and how rapidly inhaled pollutant particles pass into the systemic circulation, we measured, in 5 healthy volunteers, the distribution of radioactivity after the inhalation of "Technegas," an aerosol consisting mainly of ultrafine (99m)Technetium-labeled carbon particles (<100 nm). Radioactivity was detected in blood already at 1 minute, reached a maximum between 10 and 20 minutes, and remained at this level up to 60 minutes. Thin layer chromatography of blood showed that in addition to a species corresponding to oxidized (99m)Tc, ie, pertechnetate, there was also a species corresponding to particle-bound (99m)Tc. Gamma camera images showed substantial radioactivity over the liver and other areas of the body. We conclude that inhaled (99m)Tc-labeled ultrafine carbon particles pass rapidly into the systemic circulation, and this process could account for the well-established, but poorly understood, extrapulmonary effects of air pollution.
              Article 0 comments Cited 115 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Ching-Hung Lin: Role: Data curation
                Chia-Yi Tseng: Role: Methodology
                Ming-Wei Chao:
                ORCID: https://orcid.org/0000-0002-1574-6425
                Role: InvestigationRole: SupervisionRole: Writing – original draftRole: Writing – review & editing
                Ying-Jan Wang: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS One
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Electronic): 1932-6203
                Publication date (Electronic): 7 December 2020
                Publication date Collection: 2020
                Volume: 15
                Issue: 12
                Electronic Location Identifier: e0243062
                Affiliations
                [1 ] Department of Bioscience Technology, Chung Yuan Christian University, Taoyuan, Taiwan
                [2 ] Department of Biomedical Engineering, Chung Yuan Christian University, Taoyuan, Taiwan
                [3 ] Center for Nanotechnology, Chung Yuan Christian University, Taoyuan, Taiwan
                National Cheng Kung University, TAIWAN
                Author notes

                Competing Interests: The authors have read the journal’s policy and have the following competing interests: Yuan Li Tong Co., Ltd. provided support for this study in the form of a grant awarded to MWC. This does not alter our adherence to PLOS ONE policies on sharing data and materials. There are no patents, products in development or marketed products associated with this research to declare.

                Author information
                https://orcid.org/0000-0002-1574-6425
                Article
                Publisher ID: PONE-D-20-07104
                DOI: 10.1371/journal.pone.0243062
                PMC ID: 7721166
                PubMed ID: 33284823
                SO-VID: e8f84257-7aee-43ed-bc67-88180ab72db9
                Copyright © © 2020 Lin et al
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 11 March 2020
                Date accepted : 16 November 2020
                Page count
                Figures: 7, Tables: 0, Pages: 12
                Funding
                Funded by: YuanLiTong Enterprise
                Award Recipient :
                Yuan Li Tong Co., Ltd. provided support for this study in the form of a grant awarded to MWC (9405). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Subject: Medicine and Health Sciences
                Subject: Clinical Medicine
                Subject: Clinical Immunology
                Subject: Allergies
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Clinical Immunology
                Subject: Allergies
                Subject: Medicine and Health Sciences
                Subject: Immunology
                Subject: Clinical Immunology
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                Subject: Cell Biology
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                Subject: Immunology
                Subject: Immune Cells
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                Subject: Biology and Life Sciences
                Subject: Physiology
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                Subject: Cytokines
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immune System
                Subject: Innate Immune System
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                Subject: Medicine and Health Sciences
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                Subject: Cytokines
                Subject: Biology and Life Sciences
                Subject: Developmental Biology
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                Subject: Mouse Models
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                Subject: Animal Studies
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                Subject: Mouse Models
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immune Response
                Subject: Inflammation
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                Subject: Clinical Medicine
                Subject: Signs and Symptoms
                Subject: Inflammation
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                Subject: Medical Conditions
                Subject: Respiratory Disorders
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                Subject: Respiratory Disorders
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                Subject: Biology and Life Sciences
                Subject: Biochemistry
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                Subject: Biogenic Amines
                Subject: Histamine
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                Subject: Cell Biology
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                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immune Cells
                Subject: White Blood Cells
                Subject: Lymphocytes
                Subject: Medicine and Health Sciences
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                Subject: Immune Cells
                Subject: White Blood Cells
                Subject: Lymphocytes
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