Respiratory Syncytial Virus Infections Enhance Cigarette Smoke Induced COPD in Mice

Foronjy, Robert; Dabo, Abdoulaye; Taggart, Clifford C.; Weldon, Sinéad; Geraghty, Patrick

doi:10.1371/journal.pone.0090567

Cited by 54 publications

(70 citation statements)

References 72 publications

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“…In addition, daily intake of Lactobacillus casei Shirota increased the cytotoxic activity of natural killer cells as well as CD16 + cells in current smokers 153 . Respiratory syncytial virus infection can lead to significant airspace enlargement and fibrosis in mice exposed to cigarette smoke, as well as heightened disease severity in mice 154 . Notably, administration of L. rhamnosus before respiratory syncytial virus infection in mice resulted in elevated antiviral responses via TLR3/RIG‐I activation 155 .…”

Section: The Role Of the Microbiome In Copdmentioning

confidence: 99%

“…153 Respiratory syncytial virus infection can lead to significant airspace enlargement and fibrosis in mice exposed to cigarette smoke, as well as heightened disease severity in mice. 154 Notably, administration of L. rhamnosus before respiratory syncytial virus infection in mice resulted in elevated antiviral responses via TLR3/RIG-I activation. 155 Although the role of microbiome in COPD needs to be further investigated, early studies have suggested an association between both lung and gut microbiota and the outcomes of disease.…”

Section: The Role Of the Microbiome In Copdmentioning

confidence: 99%

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Microbiome effects on immunity, health and disease in the lung

et al. 2017

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Chronic respiratory diseases, including asthma, chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF), are among the leading causes of mortality and morbidity worldwide. In the past decade, the interest in the role of microbiome in maintaining lung health and in respiratory diseases has grown exponentially. The advent of sophisticated multiomics techniques has enabled the identification and characterisation of microbiota and their roles in respiratory health and disease. Furthermore, associations between the microbiome of the lung and gut, as well as the immune cells and mediators that may link these two mucosal sites, appear to be important in the pathogenesis of lung conditions. Here we review the recent evidence of the role of normal gastrointestinal and respiratory microbiome in health and how dysbiosis affects chronic pulmonary diseases. The potential implications of host and environmental factors such as age, gender, diet and use of antibiotics on the composition and overall functionality of microbiome are also discussed. We summarise how microbiota may mediate the dynamic process of immune development and/or regulation focusing on recent data from both clinical human studies and translational animal studies. This furthers the understanding of the pathogenesis of chronic pulmonary diseases and may yield novel avenues for the utilisation of microbiota as potential therapeutic interventions.

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Section: The Role Of the Microbiome In Copdmentioning

confidence: 99%

Section: The Role Of the Microbiome In Copdmentioning

confidence: 99%

Microbiome effects on immunity, health and disease in the lung

et al. 2017

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“…Several studies have reported that exacerbation with bacteria ( H. influenzae ), virus (rhinovirus), or a surrogate for virus-induced innate immunity (poly(I:C)) accelerates the progression of cigarette smoke-induced emphysema in mice (Foronjy, et al, 2014, Ganesan, et al, 2014, Kang, et al, 2008, Tanabe, et al, 2013). In addition, mice exposed to cigarette smoke and then infected with influenza virus H1N1 or H3N1 had increased in the number of immune cells in the BAL fluid and a 10-fold increase in lung virus titers (Bauer, et al, 2010, Gualano, et al, 2008).…”

Section: Innate and Adaptive Immunity In The Pathogenesis Of Emphymentioning

confidence: 99%

Immune-mediated inflammation in the pathogenesis of emphysema: insights from mouse models

2017

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The cellular mechanisms that result in the initiation and progression of emphysema are clearly complex. A growing body of human data combined with discoveries from mouse models utilizing cigarette smoke exposure or protease administration have improved our understanding of emphysema development by implicating specific cell types that may be important for the pathophysiology of COPD. The most important aspects of emphysematous damage appear to be oxidative or protease stress and sustained macrophage activation and infiltration of other immune cells leading to epithelial damage and cell death. Despite the identification of these associated processes and cell types in many experimental studies, the reasons why cigarette smoke and other pollutants result in unremitting damage instead of injury resolution are still uncertain. We propose an important role for macrophages in the sequence of events that lead and maintain this chronic tissue pathologic process in emphysema. This model involves chronic activation of macrophage subtypes that precludes proper healing of the lung. Further elucidation of the cross-talk between epithelial cells that release damage-associated signals and the cellular immune effectors that respond to these cues is a critical step in the development of novel therapeutics that can restore proper lung structure and function to those afflicted with emphysema.

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“…Кроме того, RSV и табачный дым синергично ак-тивировали апоптоз респираторного эпителия и подавляли экс-прессию фосфатаз, оказывающих противовоспалительное и ан-типротеазное действие. В результате сочетание этих двух пато-генных факторов приводило к выраженному фиброзу и ремоде-лированию дыхательных путей [49].…”

Section: терапевтический архив 3 2015unclassified