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      Particulate matter (PM 10) enhances RNA virus infection through modulation of innate immune responses ☆

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Sensing of pathogens by specialized receptors is the hallmark of the innate immunity. Innate immune response also mounts a defense response against various allergens and pollutants including particulate matter present in the atmosphere. Air pollution has been included as the top threat to global health declared by WHO which aims to cover more than three billion people against health emergencies from 2019 to 2023. Particulate matter (PM), one of the major components of air pollution, is a significant risk factor for many human diseases and its adverse effects include morbidity and premature deaths throughout the world. Several clinical and epidemiological studies have identified a key link between the PM existence and the prevalence of respiratory and inflammatory disorders. However, the underlying molecular mechanism is not well understood. Here, we investigated the influence of air pollutant, PM 10 (particles with aerodynamic diameter less than 10 μm) during RNA virus infections using highly pathogenic avian influenza (HPAI) – H5N1 virus. We thus characterized the transcriptomic profile of lung epithelial cell line, A549 treated with PM 10 prior to H5N1infection, which is known to cause severe lung damage and respiratory disease. We found that PM 10 enhances vulnerability (by cellular damage) and regulates virus infectivity to enhance overall pathogenic burden in the lung cells. Additionally, the transcriptomic profile highlights the connection of host factors related to various metabolic pathways and immune responses which were dysregulated during virus infection. Collectively, our findings suggest a strong link between the prevalence of respiratory illness and its association with the air quality.

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          Highlights

          • •

            Air pollution skews innate immunity during RNA virus (Influenza virus) infection.

          • •

            Particulate matter (PM10) suppresses anti-viral innate immunity.

          • •

            PM10 enhances Influenza virus replication via metabolic pathway genes modulation.

          • •

            PM10 enhances the severity of respiratory tract viral infection.

          Abstract

          Particulate matter (PM 10) enhances severity of influenza virus infection through skewing innate immunity via modulation of metabolic pathways-related genes.

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          SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor

          Markus Hoffmann, Hannah Kleine-Weber, Simon Schroeder … (2020)
          Summary The recent emergence of the novel, pathogenic SARS-coronavirus 2 (SARS-CoV-2) in China and its rapid national and international spread pose a global health emergency. Cell entry of coronaviruses depends on binding of the viral spike (S) proteins to cellular receptors and on S protein priming by host cell proteases. Unravelling which cellular factors are used by SARS-CoV-2 for entry might provide insights into viral transmission and reveal therapeutic targets. Here, we demonstrate that SARS-CoV-2 uses the SARS-CoV receptor ACE2 for entry and the serine protease TMPRSS2 for S protein priming. A TMPRSS2 inhibitor approved for clinical use blocked entry and might constitute a treatment option. Finally, we show that the sera from convalescent SARS patients cross-neutralized SARS-2-S-driven entry. Our results reveal important commonalities between SARS-CoV-2 and SARS-CoV infection and identify a potential target for antiviral intervention.
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            Association between short-term exposure to air pollution and COVID-19 infection: Evidence from China

            Zhu Yongjian, Xie Jingu, Huang Fengming … (2020)
            The novel coronavirus pneumonia, namely COVID-19, has become a global public health problem. Previous studies have found that air pollution is a risk factor for respiratory infection by carrying microorganisms and affecting body's immunity. This study aimed to explore the relationship between ambient air pollutants and the infection caused by the novel coronavirus. Daily confirmed cases, air pollution concentration and meteorological variables in 120 cities were obtained from January 23, 2020 to February 29, 2020 in China. We applied a generalized additive model to investigate the associations of six air pollutants (PM2.5, PM10, SO2, CO, NO2 and O3) with COVID-19 confirmed cases. We observed significantly positive associations of PM2.5, PM10, NO2 and O3 in the last two weeks with newly COVID-19 confirmed cases. A 10-μg/m3 increase (lag0–14) in PM2.5, PM10, NO2, and O3 was associated with a 2.24% (95% CI: 1.02 to 3.46), 1.76% (95% CI: 0.89 to 2.63), 6.94% (95% CI: 2.38 to 11.51), and 4.76% (95% CI: 1.99 to 7.52) increase in the daily counts of confirmed cases, respectively. However, a 10-μg/m3 increase (lag0–14) in SO2 was associated with a 7.79% decrease (95% CI: −14.57 to −1.01) in COVID-19 confirmed cases. Our results indicate that there is a significant relationship between air pollution and COVID-19 infection, which could partially explain the effect of national lockdown and provide implications for the control and prevention of this novel disease.
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              Fine particulate air pollution and mortality in 20 U.S. cities, 1987-1994.

              Jonathan M. Samet, Francesca Dominici, Frank C Curriero … (2000)
              Air pollution in cities has been linked to increased rates of mortality and morbidity in developed and developing countries. Although these findings have helped lead to a tightening of air-quality standards, their validity with respect to public health has been questioned. We assessed the effects of five major outdoor-air pollutants on daily mortality rates in 20 of the largest cities and metropolitan areas in the United States from 1987 to 1994. The pollutants were particulate matter that is less than 10 microm in aerodynamic diameter (PM10), ozone, carbon monoxide, sulfur dioxide, and nitrogen dioxide. We used a two-stage analytic approach that pooled data from multiple locations. After taking into account potential confounding by other pollutants, we found consistent evidence that the level of PM10 is associated with the rate of death from all causes and from cardiovascular and respiratory illnesses. The estimated increase in the relative rate of death from all causes was 0.51 percent (95 percent posterior interval, 0.07 to 0.93 percent) for each increase in the PM10 level of 10 microg per cubic meter. The estimated increase in the relative rate of death from cardiovascular and respiratory causes was 0.68 percent (95 percent posterior interval, 0.20 to 1.16 percent) for each increase in the PM10 level of 10 microg per cubic meter. There was weaker evidence that increases in ozone levels increased the relative rates of death during the summer, when ozone levels are highest, but not during the winter. Levels of the other pollutants were not significantly related to the mortality rate. There is consistent evidence that the levels of fine particulate matter in the air are associated with the risk of death from all causes and from cardiovascular and respiratory illnesses. These findings strengthen the rationale for controlling the levels of respirable particles in outdoor air.
              Article 0 comments Cited 407 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Himanshu Kumar
                Journal
                Journal ID (nlm-ta): Environ Pollut
                Journal ID (iso-abbrev): Environ. Pollut
                Title: Environmental Pollution (Barking, Essex : 1987)
                Publisher: Elsevier Ltd.
                ISSN (Print): 0269-7491
                ISSN (Electronic): 1873-6424
                Publication date PMC-release: 13 July 2020
                Publication date (Electronic): 13 July 2020
                Electronic Location Identifier: 115148
                Affiliations
                [a ]Department of Biological Sciences, Laboratory of Immunology and Infectious Disease Biology, Indian Institute of Science Education and Research (IISER) Bhopal, Bhopal, 462066, MP, India
                [b ]National Institute of Technology Karnataka (NITK), Surathkal, Mangaluru, 575025, Karnataka, India
                [c ]Centre for Water Food and Environment, IIT Ropar, Rupnagar, 140001, Punjab, India
                [d ]Pathogenomics Laboratory, ICAR – National Institute of High Security Animal Diseases (NIHSAD), OIE Reference Laboratory for Avian Influenza, Bhopal, 462021, MP, India
                [e ]WPI Immunology, Frontier Research Centre, Osaka University, Osaka, 5650871, Japan
                Author notes
                [∗ ]Corresponding author. Department of Biological Sciences, Laboratory of Immunology and Infectious Disease Biology, Indian Institute of Science Education and Research (IISER) Bhopal, AB-3, Room No. 220, Bhopal By-pass Road, Bhauri, Bhopal, 462066, MP, India. hkumar@ 123456iiserb.ac.in
                Article
                Publisher ID: S0269-7491(20)32561-6 Publisher ID: 115148
                DOI: 10.1016/j.envpol.2020.115148
                PMC ID: 7357538
                PubMed ID: 32771845
                SO-VID: 8bb5432c-27d7-4491-ad09-8978e3a69de3
                Copyright © © 2020 Elsevier Ltd. All rights reserved.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                Date received : 8 April 2020
                Date revision received : 28 June 2020
                Date accepted : 28 June 2020
                Categories
                Subject: Article

                ScienceOpen disciplines: General environmental science
                Keywords: air pollution,pm10,viral infection,anti-viral innate immunity,metabolic pathways genes
                Data availability:
                ScienceOpen disciplines: General environmental science
                Keywords: air pollution, pm10, viral infection, anti-viral innate immunity, metabolic pathways genes

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