In utero tobacco smoke exposure alters lung inflammation, viral clearance, and CD8<sup>+</sup>T-cell responses in neonatal mice infected with respiratory syncytial virus

Cheemarla, Nagarjuna R.; Uche, Ifeanyi K.; McBride, Kaitlin; Naidu, Shan K.; Guerrero-Plata, Antonieta

doi:10.1152/ajplung.00338.2018

Cited by 8 publications

(7 citation statements)

References 74 publications

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“…Smoking exposure during pregnancy may cause disease by altering RSV and changing neonatal immune responses, which can increase the risk of respiratory tract infection. Cheemarla et al 120 showed that intrauterine smoke exposure in a mouse model led to increased lung inflammation, with increased neutrophil influx into the airway of infected mice and delayed virus clearing; however, the authors found that RSV-specific CD8 + T cells had a decreased response.…”

Section: Smoking and Infection With Different Respiratory Pathogensmentioning

confidence: 99%

Smoking increases the risk of infectious diseases: A narrative review

Chen¹,

Chen²,

Xie³

2020

Tob. Induc. Dis.

114

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Smoking is one of the most severe public health problems in the world. According to the WHO Global report on trends in prevalence of tobacco use 2000-2025, smoking accounts for 9% of all deaths worldwide, and more than half of smokers die from smoking-related diseases 1. China is the largest producer and consumer of tobacco in the world. In 2018, about 26.6% of adults (aged ≥15 years; 308 million in total) were current smokers and 44.9% of adults (515 million) were exposed to secondhand smoke at home 1. Exposure to cigarette smoke and secondhand smoke is very harmful to human health. There are over 7000 chemical components in tobacco smoke, of these, over 250 are toxic or carcinogenic, such as aldehydes, nitrides, and others that irritate the respiratory tract. Nicotine leads to tobacco addiction; benzpyrene, arsenic, cadmium and other components have carcinogenic effects and nitric oxide can reduce oxygen transport by erythrocytes. Smoking can damage nearly all organs of the human body and is one of the main risk factors for respiratory infection and infectious diseases in other systems, in a dose-dependent manner 2,3. In this review, we discuss the mechanisms and influence of smoking on infections in various systems, including the respiratory system, digestive system, and genital system, among others, in order to provide evidence for the active promotion of smoking cessation. DEVELOPMENTS Mechanisms of susceptibility The potential mechanisms of how cigarette smoke increases the risk of systemic infections are not completely understood. These may include alteration ABSTRACT Smoking is relevant to infectious diseases resulting in increased prevalence and mortality. In this article, we aim to provide an overview of the effects of smoking in various infections and to explain the potential mechanisms. We searched PubMed and other relevant databases for scientific studies that explored the relationship between smoking and infection. The mechanisms of susceptibility to infection in smokers may include alteration of the structural, functional and immunologic host defences. Smoking is one of the main risk factors for infections in the respiratory tract, digestive tract, reproductive tract, and other systems in humans, increasing the prevalence of HIV, tuberculosis, SARS-CoV, and the current SARS-CoV-2. Smoking cessation can reduce the risk of infection. Smoking increases the incidence of infections and aggravates the progress and prognosis of infectious diseases in a dose-dependent manner. Smoking cessation promotion and education are the most practical and economical preventive measures to reduce aggravation of disease infection owing to tobacco use.

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Section: Smoking and Infection With Different Respiratory Pathogensmentioning

confidence: 99%

Smoking increases the risk of infectious diseases: A narrative review

Chen¹,

Chen²,

Xie³

2020

Tob. Induc. Dis.

114

View full text Add to dashboard Cite

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“…CS exposure reportedly leads to increased neutrophilic inflammation in the airways, and delayed viral clearance due to a reduced respiratory syncytial virus-specific CD8+ T cell response [70]. In another study mice exposed to CS recovered poorly from primary Influenza A pneumonia with reduced type I and II IFNs and virus-specific immunoglobulins [71].…”

Section: Discussionmentioning

confidence: 97%

The traditional herbal formulation, Jianpiyifei II, reduces pulmonary inflammation induced by influenza A virus and cigarette smoke in mice

Cai

Liu

et al. 2021

Clinical Science

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Chronic obstructive pulmonary disease (COPD) is a worldwide chronic inflammatory lung disease, and influenza A virus (IAV) infection is a common cause of acute exacerbations of COPD (AECOPD). Therefore, targeting viral infections represents a promising strategy to prevent the occurrence and development of inflammatory flare ups in AECOPD. Jianpiyifei II (JPYFII) is a traditional herbal medicine used in China to treat patients with COPD, and its clinical indications are not well understood. However, investigation of the anti-inflammatory effects and underlying mechanism using an animal model of smoking has been reported in a previous study by our group. In addition, some included herbs, such as Radix astragali and Radix aupleuri, were reported to exhibit anti-viral effects. Therefore, the aim of this study was to investigate whether JPYFII formulation relieved acute inflammation by clearing the IAV in a mouse model that was exposed to cigarette smoke experimentally. JPYFII formulation treatment during smoke exposure and IAV infection significantly reduced the number of cells observed in bronchoalveolar lavage fluid (BALF), expression of pro-inﬂammatory cytokines, chemokines, superoxide production, and viral load in IAV-infected and smoke-exposed mice. However, JPYFII formulation treatment during smoke exposure alone did not reduce the number of cells in BALF or the expression of Il-6, Tnf-a, and Il-1β. The results demonstrated that JPYFII formulation exerted an anti-viral effect and reduced the exacerbation of lung inflammation in cigarette smoke (CS)-exposed mice infected with IAV. Our results suggested that JPYFII formulation could potentially be used to treat patients with AECOPD associated with IAV infection.

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“…61 Pathologically, severe bronchiolitis has the features of neutrophilic inflammatory response, mucus hypersecretion, shedding of airway epithelial cells, etc., epithelial cell death with viscous exudate, may constitute a dense plug within the bronchiolar lumen, impeding breathing. 62,63 RSV-mediated death of airway epithelial cells is connected to elevated phosphorylation of RIPK1 and MLKL but not activated caspase-3. 64 Meanwhile, RSV infection induces the early release of HMGB1 that further facilitates the late phase of HMGB1 release through activation of RAGE, with subsequent cell death.…”

Section: Inflammationmentioning

confidence: 99%

“…In addition, severe RSV bronchiolitis in infancy contributes to airway diseases, for example, asthma 61 . Pathologically, severe bronchiolitis has the features of neutrophilic inflammatory response, mucus hypersecretion, shedding of airway epithelial cells, etc., epithelial cell death with viscous exudate, may constitute a dense plug within the bronchiolar lumen, impeding breathing 62,63 . RSV‐mediated death of airway epithelial cells is connected to elevated phosphorylation of RIPK1 and MLKL but not activated caspase‐3 64 .…”

Section: The Key Molecular Mechanisms Underlying Necroptosis Of Speci...mentioning

confidence: 99%

Cell type‐specific molecular mechanisms and implications of necroptosis in inflammatory respiratory diseases

Guo,

Zhou,

Wang

et al. 2023

Immunological Reviews

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SummaryNecroptosis is generally considered as an inflammatory cell death form. The core regulators of necroptotic signaling are receptor‐interacting serine–threonine protein kinases 1 (RIPK1) and RIPK3, and the executioner, mixed lineage kinase domain‐like pseudokinase (MLKL). Evidence demonstrates that necroptosis contributes profoundly to inflammatory respiratory diseases that are common public health problem. Necroptosis occurs in nearly all pulmonary cell types in the settings of inflammatory respiratory diseases. The influence of necroptosis on cells varies depending upon the type of cells, tissues, organs, etc., which is an important factor to consider. Thus, in this review, we briefly summarize the current state of knowledge regarding the biology of necroptosis, and focus on the key molecular mechanisms that define the necroptosis status of specific cell types in inflammatory respiratory diseases. We also discuss the clinical potential of small molecular inhibitors of necroptosis in treating inflammatory respiratory diseases, and describe the pathological processes that engage cross talk between necroptosis and other cell death pathways in the context of respiratory inflammation. The rapid advancement of single‐cell technologies will help understand the key mechanisms underlying cell type‐specific necroptosis that are critical to effectively treat pathogenic lung infections and inflammatory respiratory diseases.

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In utero tobacco smoke exposure alters lung inflammation, viral clearance, and CD8⁺T-cell responses in neonatal mice infected with respiratory syncytial virus

Cited by 8 publications

References 74 publications

Smoking increases the risk of infectious diseases: A narrative review

Smoking increases the risk of infectious diseases: A narrative review

The traditional herbal formulation, Jianpiyifei II, reduces pulmonary inflammation induced by influenza A virus and cigarette smoke in mice

Cell type‐specific molecular mechanisms and implications of necroptosis in inflammatory respiratory diseases

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In utero tobacco smoke exposure alters lung inflammation, viral clearance, and CD8+T-cell responses in neonatal mice infected with respiratory syncytial virus

Cited by 8 publications

References 74 publications

Smoking increases the risk of infectious diseases: A narrative review

Smoking increases the risk of infectious diseases: A narrative review

The traditional herbal formulation, Jianpiyifei II, reduces pulmonary inflammation induced by influenza A virus and cigarette smoke in mice

Cell type‐specific molecular mechanisms and implications of necroptosis in inflammatory respiratory diseases

Contact Info

Product

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In utero tobacco smoke exposure alters lung inflammation, viral clearance, and CD8⁺T-cell responses in neonatal mice infected with respiratory syncytial virus