Cigarette smoke attenuates the RIG-I-initiated innate antiviral response to influenza infection in two murine models

Wu, Wenxin; Zhang, Wei; More, Sunil S.; Booth, J. Leland; Duggan, Elizabeth S.; Liu, Lin; Zhao, Yan; Metcalf, Jordan P.

doi:10.1152/ajplung.00158.2014

Cited by 19 publications

(30 citation statements)

References 33 publications

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“…In addition, CS represses phagocytosis of pathogens by alveolar macrophages (Drannik et al 2004;Marti-Lliteras et al 2009;Phipps et al 2010) and the activity of the toll-like and nucleotide oligomerization domain receptors, TLR3, TLR4, NOD1, and NOD2 in these cells (Droemann et al 2005;Gaschler et al 2008;Hristova et al 2012). CS also represses antiviral immunity by impairing RIG-I activation (Wu et al 2014). The data here add to these findings by showing that cigarette smoke represses mediators of innate immunity that respond to inhaled asbestos, including IL-18 and IL-33.…”

Section: Discussionsupporting

confidence: 55%

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Cigarette smoke represses the innate immune response to asbestos

Morris¹,

Danchuk²,

Wang³

et al. 2015

Physiol Rep

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Both cigarette smoke (CS) and asbestos cause lung inflammation and lung cancer, and at high asbestos exposure levels, populations exposed to both of these carcinogens display a synergistic increase in the development of lung cancer. The mechanisms through which these two toxic agents interact to promote lung tumorigenesis are poorly understood. Here, we begin to dissect the inflammatory signals induced by asbestos in combination with CS using a rodent inhalation model and in vitro cell culture. Wild‐type C57BL/6 mice were exposed to room air as a control, CS, and/or asbestos (4 days per week to CS and 1 day per week to asbestos for 5 weeks). Bronchoalveolar lavage (BAL) fluid was collected following exposure and analyzed for inflammatory mediators. Asbestos‐exposed mice displayed an increased innate immune response consistent with NLRP3 inflammasome activation. Compared to mice exposed only to asbestos, animals coexposed to CS + asbestos displayed attenuated levels of innate immune mediators and altered inflammatory cell recruitment. Histopathological changes in CS + asbestos‐exposed mice correlated with attenuated fibroproliferative lesion development relative to their counterparts exposed only to asbestos. In vitro experiments using a human monocyte cell line (THP‐1 cells) supported the in vivo results in that coexposure to cigarette smoke extract repressed NLRP3 inflammasome markers in cells treated with asbestos. These observations indicate that CS represses central components of the innate immune response to inhaled asbestos.

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Section: Discussionsupporting

confidence: 55%

“…CS also represses antiviral immunity by impairing RIG‐I activation (Wu et al. ). The data here add to these findings by showing that cigarette smoke represses mediators of innate immunity that respond to inhaled asbestos, including IL‐18 and IL‐33.…”

Section: Discussionmentioning

confidence: 99%

Cigarette smoke represses the innate immune response to asbestos

Morris¹,

Danchuk²,

Wang³

et al. 2015

Physiol Rep

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“…For determination of viral titers in infected mice, whole mouse lungs were collected and homogenized in 1 ml of ice cold PBS. Solid debris was pelleted by centrifugation and viral titer was determined using a standard plaque assay on MDCK cells [ 22 ]. Results were expressed as PFU/ml of extract.…”

Section: Methodsmentioning

confidence: 99%

“…Whole-body CS exposure was performed as described [ 22 ]. Mice were exposed to the smoke of 3R4F reference cigarettes (University of Kentucky, Lexington, KY) for 5 h per day.…”

Section: Methodsmentioning

confidence: 99%

RIG-I overexpression decreases mortality of cigarette smoke exposed mice during influenza A virus infection

Wang

Zhang

et al. 2017

Respir Res

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BackgroundRetinoic acid-inducible gene I (RIG-I) is an important regulator of virus-induced antiviral interferons (IFNs) and proinflammatory cytokines which participate in clearing viral infections. Cigarette smoke (CS) exposure increases the frequency and severity of respiratory tract infections.MethodsWe generated a RIG-I transgenic (TG) mouse strain that expresses the RIG-I gene product under the control of the human lung specific surfactant protein C promoter. We compared the mortality and host immune responses of RIG-I TG mice and their litter-matched wild type (WT) mice following challenge with influenza A virus (IAV).ResultsRIG-I overexpression increased survival of IAV-infected mice. CS exposure increased mortality in WT mice infected with IAV. Remarkably, the effect of RIG-I overexpression on survival during IAV infection was enhanced in CS-exposed animals. CS-exposed IAV-infected WT mice had a suppressed innate response profile in the lung compared to sham-exposed IAV-infected WT mice in terms of the protein concentration, total cell count and inflammatory cell composition in the bronchoalveolar lavage fluid. RIG-I overexpression restored the innate immune response in CS-exposed mice to that seen in sham-exposed WT mice during IAV infection, and is likely responsible for enhanced survival in RIG-I TG mice as restoration preceded death of the animals.ConclusionsOur results demonstrate that RIG-I overexpression in mice is protective for CS enhanced susceptibility of smokers to influenza infection, and that CS mediated RIG-I suppression may be partially responsible for the increased morbidity and mortality of the mice exposed to IAV. Thus, optimizing the RIG-I response may be an important treatment strategy for CS-enhanced lung infections, particularly those due to IAV.

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“…In the case of whole cigarette smoke extract and the tar phase extract, concentrations have been expressed in terms of the concentrations of endogenous substances such as nicotine [27][28][29] : the amount of these substances is relatively easy to determine using gas chromatography or the weight trapped on the Cambridge filter, respectively. However, in the case of nicotine-and tar-free CSE, it is difficult to express its concentration, because it does not contain appropriate endogenous substances like nicotine and tar.…”

Section: Expression Of the Concentration Of Csementioning

confidence: 99%

A Standardized Method for the Preparation of a Gas Phase Extract of Cigarette Smoke

Higashi

Mai

Mazaki

et al. 2016

Biological & Pharmaceutical Bulletin

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The gas phase of cigarette smoke is important from the viewpoint of human health, because it can pass through alveolar epithelium and enter the circulation. There is no standard method for the preparation of a gas phase extract of cigarette smoke (CSE), although CSE is widely used for research instead of whole cigarette smoke. We have established a standard method for the preparation of CSE. One cigarette per trial is continuously combusted under a reduced pressure generated by an aspiration pump with a velocity of 1.050 L/min: the main stream of the smoke is passed through a Cambridge filter to remove tar, and subsequently, bubbled through a glass ball filter (pore size, 20-30 µm) into 15 mL of phosphate-buffered saline (PBS). To express the concentration of CSE, a virtual tar concentration is introduced, which is calculated assuming that tar trapped on the Cambridge filter is dissolved in the PBS. CSEs prepared from smaller numbers of cigarettes (original virtual tar concentration≤15 mg/mL) show similar concentration-response curves for cytotoxicity versus virtual tar concentrations. CSEs prepared from various brands of cigarettes and by different smoking regimes (continuous and puff smoking) show similar cytotoxic potency if the virtual tar concentrations are the same. In conclusion, using the standardized method for CSE preparation in combination with the virtual tar concentration, it becomes possible to simply and rapidly prepare standard CSEs with defined concentrations from any brand of cigarettes, which are toxicologically equivalent to CSE prepared by puff smoking.

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Cigarette smoke attenuates the RIG-I-initiated innate antiviral response to influenza infection in two murine models

Abstract: Cigarette smoke attenuates the RIG-I-initiated innate antiviral response to influenza infection in two murine models.

Cited by 19 publications

References 33 publications

Cigarette smoke represses the innate immune response to asbestos

Cigarette smoke represses the innate immune response to asbestos

RIG-I overexpression decreases mortality of cigarette smoke exposed mice during influenza A virus infection

A Standardized Method for the Preparation of a Gas Phase Extract of Cigarette Smoke

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