Depression of viral interferon induction in cell monolayers by coal dust

Hahon, Nicholas

doi:10.1136/oem.31.3.201

Cited by 9 publications

(11 citation statements)

References 18 publications

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“…197 Coal dust suppressed virus-induced IFN induction. 198 Chronic aerosol exposure to diesel engine exhaust resulted in increased influenza viral growth in lungs and decreased IFN and antibody levels. 199 Ma et al observed differential effects in mice acutely or chronically exposed to PM; chronic exposure reduced pulmonary resistance to influenza A virus infection and downregulated levels of histone demethylase KDM6A, altering histone methylation patterns on the IFN-β and IL-6 promoters, while acute exposure increased the production of IFN-β, IL-6, and OAS1.…”

Section: Potential Effects Of Pollutant Exposure On Viral Replicationmentioning

confidence: 99%

SARS‐CoV‐2 infection, COVID‐19 pathogenesis, and exposure to air pollution: What is the connection?

Woodby

Arnold

Valacchi

2020

Annals of the New York Academy of Sciences

131

113

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Exposure to air pollutants has been previously associated with respiratory viral infections, including influenza, measles, mumps, rhinovirus, and respiratory syncytial virus. Epidemiological studies have also suggested that air pollution exposure is associated with increased cases of SARS-CoV-2 infection and COVID-19-associated mortality, although the molecular mechanisms by which pollutant exposure affects viral infection and pathogenesis of COVID-19 remain unknown. In this review, we suggest potential molecular mechanisms that could account for this association. We have focused on the potential effect of exposure to nitrogen dioxide (NO 2), ozone (O 3), and particulate matter (PM) since there are studies investigating how exposure to these pollutants affects the life cycle of other viruses. We have concluded that pollutant exposure may affect different stages of the viral life cycle, including inhibition of mucociliary clearance, alteration of viral receptors and proteases required for entry, changes to antiviral interferon production and viral replication, changes in viral assembly mediated by autophagy, prevention of uptake by macrophages, and promotion of viral spread by increasing epithelial permeability. We believe that exposure to pollutants skews adaptive immune responses toward bacterial/allergic immune responses, as opposed to antiviral responses. Exposure to air pollutants could also predispose exposed populations toward developing COIVD-19associated immunopathology, enhancing virus-induced tissue inflammation and damage.

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Section: Potential Effects Of Pollutant Exposure On Viral Replicationmentioning

confidence: 99%

SARS‐CoV‐2 infection, COVID‐19 pathogenesis, and exposure to air pollution: What is the connection?

Woodby

Arnold

Valacchi

2020

Annals of the New York Academy of Sciences

131

113

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“…LLC-MK2 cell monolayers grown in plastic tissue culture flasks (75 cm 2) and treated with ultraviolet-irradiated PI%8 influenza virus provided the source of interferon preparations (3). The preparations possessed the biological and physical properties ascribed to interferon (11).…”

Section: Inter/eronmentioning

confidence: 99%

Interferon assessment by the immunofluorescent, immunoperoxidase, and hemadsorption cell-counting techniques

Hahon

Booth

Eckert

1975

Archives of Virology

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“…Studies of the induction of interferon by influenza virus in cell Received for publication 30 June 1976 Accepted for publication 9 September 1976 monolayers have shown that this adaptive cellular response was depressed, partially or completely, in the presence of either coal dust or serpentine and amphibole asbestos fibres (Hahon, 1974;Hahon and Eckert, 1976). Furthermore, virus multiplication was slightly enhanced in cell cultures pretreated with these mineral dusts.…”

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confidence: 99%

Antagonistic activity of poly (4-vinylpyridine-N-oxide) to the inhibition of viral interferon induction by asbestos fibres.

Hahon¹,

Booth²,

Eckert³

1977

Occupational and Environmental Medicine

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The depressive activity of both serpentine (Canadian and Rhodesian chrysotiles) and amphibole (amosite, crocidolite, and anthophyllite) asbestos fibres on interferon induction by influenza virus was significantly diminished or abolished completely when either asbestos fibres or LLC-MK2 cell monolayers were pretreated with poly(4-vinylpyridine-N-oxide). Maximal antagonistic activity of the polymer was time and concentration dependent. Pretreating asbestos fibres with the polymer was more rapid and effective in encouraging viral interferon synthesis than pretreating cell monolayers. Virus multiplication in the presence of asbestos fibre-treated cell monolayers attained a twofold higher level than that noted in normal cell monolayers or those containing polymer-pretreated asbestos fibres. These findings were related to the suppression of interferon production.The protection afforded by poly(vinylpyridine-Noxides) and related polymers against the fibrogenic and cytotoxic activities of silica (Schlipk6ter and Brockhaus, 1961;Beck et al., 1963) is a promising advance in pneumoconiosis research that may have an application in the field of chemoprophylaxis (Holt, 1971). Although they are effective inhibitors of haemolysis by silica, the poly(vinylpyridine oxides) have little effect in preventing haemolysis by the serpentine form of asbestos (Macnab and Harington, 1967;Harington et al., 1971). Under specified conditions, however, the polymer has been reported to counteract haemolysis by amphibole asbestiform fibres such as anthophyllite (Schnitzer et al., 1971;Harington et al., 1971). Although haemolysis of erythrocytes plays no part in the pathogenesis of pneumoconiosis, this in vitro phenomenon has been used to study the effects of mineral dusts on biological membranes (Harington etal., 1975).Mineral dusts may challenge the integrity and efficacy of the interferon system. Studies of the induction of interferon by influenza virus in cell Received for publication 30 June 1976 Accepted for publication 9 September 1976 monolayers have shown that this adaptive cellular response was depressed, partially or completely, in the presence of either coal dust or serpentine and amphibole asbestos fibres (Hahon, 1974;Hahon and Eckert, 1976). Furthermore, virus multiplication was slightly enhanced in cell cultures pretreated with these mineral dusts. Because the interferon system is responsive to the effects of mineral dusts, amenable to quantitative assessment, and an integral component of nonimmunological cellular defence, it is a valuable indicator for studies on experimental infective pneumoconiosis at the cellular level.A recent study has shown that the depressive activity of coal dust on viral interferon induction was markedly counteracted when either coal dust or cell monolayers were pretreated with poly (4-vinylpyridine-N-oxide) (PVPNO) .The polymer alone neither induced interferon, inhibited viral induction of interferon, influenced virus replication, nor affected cellular-induced resistance by interferon. In...

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Depression of viral interferon induction in cell monolayers by coal dust

Cited by 9 publications

References 18 publications

SARS‐CoV‐2 infection, COVID‐19 pathogenesis, and exposure to air pollution: What is the connection?

SARS‐CoV‐2 infection, COVID‐19 pathogenesis, and exposure to air pollution: What is the connection?

Interferon assessment by the immunofluorescent, immunoperoxidase, and hemadsorption cell-counting techniques

Antagonistic activity of poly (4-vinylpyridine-N-oxide) to the inhibition of viral interferon induction by asbestos fibres.

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