Development of an experimental model for assessing the effects of cigarette smoke and virus infections on inflammatory responses to bacterial antigens

Determining the role of NADPH oxidases in the context of virus infection is an emerging area of research and our knowledge is still sparse. The expression of various isoforms of NOX/DUOX (NADPH oxidase/dual oxidase) in the epithelial cells (ECs) lining the respiratory tract renders them primary sites from which to orchestrate the host defence against respiratory viruses. Accumulating evidence reveals distinct facets of the involvement of NOX/DUOX in host antiviral and pro-inflammatory responses and in the control of the epithelial barrier integrity, with individual isoforms mediating co-operative, but surprisingly also opposing, functions. Although in vivo studies in mice are in line with some of these observations, a complete understanding of the specific functions of epithelial NOX/DUOX awaits lung epithelial-specific conditional knockout mice. The goal of the present review is to summarize our current knowledge of the role of individual NOX/DUOX isoforms expressed in the lung epithelium in the context of respiratory virus infections so as to highlight potential opportunities for therapeutic intervention.

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Inflammatory responses bridge comorbid cardiac disorder in experimental model of IBD induced by DSS: protective effect of the trigonelline

Inflammopharmacology ◽

10.1007/s10787-019-00581-w ◽

2019 ◽

Vol 27 (6) ◽

pp. 1265-1273 ◽

Cited By ~ 3

Author(s):

Hossein Omidi-Ardali ◽

Zahra Lorigooini ◽

Amin Soltani ◽

Shima Balali-Dehkordi ◽

Hossein Amini-Khoei

Keyword(s):

Protective Effect ◽

Experimental Model ◽

Inflammatory Responses ◽

Cardiac Disorder

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Association of modulation of pro‐inflammatory responses by dectin‐2 with preterm delivery: An experimental model

American Journal of Reproductive Immunology ◽

10.1111/aji.13216 ◽

2020 ◽

Vol 83 (3) ◽

Author(s):

Aspasia Liassidou ◽

Georgios Renieris ◽

Dionysia‐Irene Droggiti ◽

Theologia Gkavogianni ◽

Christakis Liassides ◽

...

Keyword(s):

Experimental Model ◽

Preterm Delivery ◽

Inflammatory Responses

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Comparison of the effects of e-cigarette vapor with cigarette smoke on lung function and inflammation in mice

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00389.2017 ◽

2018 ◽

Vol 315 (5) ◽

pp. L662-L672 ◽

Cited By ~ 37

Author(s):

Constantinos Glynos ◽

Sofia-Iris Bibli ◽

Paraskevi Katsaounou ◽

Athanasia Pavlidou ◽

Christina Magkou ◽

...

Keyword(s):

Oxidative Stress ◽

Cigarette Smoke ◽

Inflammatory Responses ◽

Electronic Cigarettes ◽

Ambient Air ◽

Lavage Fluid ◽

Pulmonary Mechanics ◽

Tissue Elasticity ◽

Stress Markers

Electronic cigarettes (e-cigs) are advertised as a less harmful nicotine delivery system or as a new smoking cessation tool. We aimed to assess the in vivo effects of e-cig vapor in the lung and to compare them to those of cigarette smoke (CS). We exposed C57BL/6 mice for either 3 days or 4 wk to ambient air, CS, or e-cig vapor containing 1) propylene glycol/vegetable glycerol (PG:VG-Sol; 1:1), 2) PG:VG with nicotine (G:VG-N), or 3) PG:VG with nicotine and flavor (PG:VG-N+F) and determined oxidative stress, inflammation, and pulmonary mechanics. E-cig vapors, especially PG:VG-N+F, increased bronchoalveolar lavage fluid (BALF) cellularity, Muc5ac production, as well as BALF and lung oxidative stress markers at least comparably and in many cases more than CS. BALF protein content at both time points studied was only elevated in the PG:VG-N+F group. After 3 days, PG:VG-Sol altered tissue elasticity, static compliance, and airway resistance, whereas after 4 wk CS was the only treatment adversely affecting these parameters. Airway hyperresponsiveness in response to methacholine was increased similarly in the CS and PG:VG-N+F groups. Our findings suggest that exposure to e-cig vapor can trigger inflammatory responses and adversely affect respiratory system mechanics. In many cases, the added flavor in e-cigs exacerbated the detrimental effects of e-cig vapor. We conclude that both e-cig vaping and conventional cigarette smoking negatively impact lung biology.

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CCR7 Modulates Pulmonary and Lymph Node Inflammatory Responses in Cigarette Smoke-Exposed Mice

The Journal of Immunology ◽

10.4049/jimmunol.0902015 ◽

2009 ◽

Vol 183 (12) ◽

pp. 8186-8194 ◽

Cited By ~ 18

Author(s):

Tine Demoor ◽

Ken R. Bracke ◽

Karim Y. Vermaelen ◽

Lisa Dupont ◽

Guy F. Joos ◽

...

Keyword(s):

Lymph Node ◽

Cigarette Smoke ◽

Inflammatory Responses

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Cigarette smoke and CFTR: implications in the pathogenesis of COPD

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00039.2013 ◽

2013 ◽

Vol 305 (8) ◽

pp. L530-L541 ◽

Cited By ~ 87

Author(s):

Andras Rab ◽

Steven M. Rowe ◽

S. Vamsee Raju ◽

Zsuzsa Bebok ◽

Sadis Matalon ◽

...

Keyword(s):

Cystic Fibrosis ◽

Cigarette Smoke ◽

Inflammatory Responses ◽

Common Mechanism ◽

Chronic Obstructive ◽

Respiratory Disorder ◽

Chronic Infections ◽

Gene Encoding ◽

Obstructive Pulmonary Disease ◽

Copd Patients

Chronic obstructive pulmonary disease (COPD) is a progressive respiratory disorder consisting of chronic bronchitis and/or emphysema. COPD patients suffer from chronic infections and display exaggerated inflammatory responses and a progressive decline in respiratory function. The respiratory symptoms of COPD are similar to those seen in cystic fibrosis (CF), although the molecular basis of the two disorders differs. CF is a genetic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator ( CFTR) gene encoding a chloride and bicarbonate channel (CFTR), leading to CFTR dysfunction. The majority of COPD cases result from chronic oxidative insults such as cigarette smoke. Interestingly, environmental stresses including cigarette smoke, hypoxia, and chronic inflammation have also been implicated in reduced CFTR function, and this suggests a common mechanism that may contribute to both the CF and COPD. Therefore, improving CFTR function may offer an excellent opportunity for the development of a common treatment for CF and COPD. In this article, we review what is known about the CF respiratory phenotype and discuss how diminished CFTR expression-associated ion transport defects may contribute to some of the pathological changes seen in COPD.

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Peroxisome proliferator-activated receptor-γ inhibits cigarette smoke solution-induced mucin production in human airway epithelial (NCI-H292) cells

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00388.2005 ◽

2006 ◽

Vol 291 (1) ◽

pp. L84-L90 ◽

Cited By ~ 38

Author(s):

Sung Yong Lee ◽

Eun Joo Kang ◽

Gyu Young Hur ◽

Ki Hwan Jung ◽

Hye Cheol Jung ◽

...

Keyword(s):

Cigarette Smoke ◽

Inflammatory Responses ◽

Cigarette Smoke Exposure ◽

Etiologic Factor ◽

Peroxisome Proliferator ◽

Cell Hyperplasia ◽

Peroxisome Proliferator Activated Receptor ◽

Mucin Production ◽

Ppar Γ ◽

Anti Inflammatory

The main etiologic factor for chronic bronchitis is cigarette smoke. Exposure to cigarette smoke is reported to induce goblet cell hyperplasia and mucus production. Mucin synthesis in airways has been reported to be regulated by the EGFR system. Peroxisome proliferator-activated receptor-γ (PPAR-γ) is a member of the ligand-activated nuclear receptor superfamily. PPAR-γ is implicated in anti-inflammatory responses, but mechanisms underlying these varied roles remain ill-defined. Recently, reports have shown that upregulation of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) might be one of the mechanisms through which PPAR-γ agonists exert their anti-inflammatory actions. However, no data are available on the role of PPAR-γ in smoke-induced mucin production. In this study, we investigated the effect of PPAR-γ agonist (rosiglitazone) on smoke-induced mucin production in NCI-H292 cells. Exposure to cigarette smoke causes a significant decrease in PTEN expression and increases dose-dependent EGFR-specific tyrosine phosphorylation, resulting in MUC5AC mucin production in NCI-H292 cells. PPAR-γ agonists or specific inhibitors of phosphoinositide 3-kinase exert inhibition of cigarette smoke-induced mucin production, with the upregulation of PTEN signaling and downregulation of Akt expression. This study demonstrates that PPAR-γ agonist functions as a regulator of epithelial cell inflammation that may result in reduction of mucin-producing cells in airway epithelium.

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