The use of electronic cigarettes (e-cigs) is increasing rapidly, but their effects on lung toxicity are largely unknown. Smoking is a well-established cause of lung cancer and respiratory disease, in part through inflammation. It is plausible that e-cig use might affect similar inflammatory pathways. E-cigs are used by some smokers as an aid for quitting or smoking reduction, and by never smokers (e.g., adolescents and young adults). The relative effects for impacting disease risk may differ for these groups. Cell culture and experimental animal data indicate that e-cigs have the potential for inducing inflammation, albeit much less than smoking. Human studies show that e-cig use in smokers is associated with substantial reductions in blood or urinary biomarkers of tobacco toxicants when completely switching and somewhat for dual use. However, the extent to which these biomarkers are surrogates for potential lung toxicity remains unclear. The FDA now has regulatory authority over e-cigs and can regulate product and e-liquid design features, such as nicotine content and delivery, voltage, e-liquid formulations, and flavors. All of these factors may impact pulmonary toxicity. This review summarizes current data on pulmonary inflammation related to both smoking and e-cig use, with a focus on human lung biomarkers. Cancer Epidemiol Biomarkers Prev; 26(8); 1175-91. ©2017 AACR.

https://cebp.aacrjournals.org/content/cebp/26/8/1175.full.pdf

A Review of Pulmonary Toxicity of Electronic Cigarettes In The Context of Smoking: A Focus On Inflammation

Chronic obstructive pulmonary disease (COPD), a common and heterogeneous respiratory disease, is characterized by persistent and incompletely reversible airflow limitation. Metabolomics is applied to analyze the difference of metabolic profile based on the low-molecular-weight metabolites (<1 kDa). Emerging metabolomic analysis may provide insights into the pathogenesis and diagnosis of COPD. This review aims to summarize the alteration of metabolites in blood/serum/plasma, urine, exhaled breath condensate, lung tissue samples, etc. from COPD individuals, thereby uncovering the potential pathogenesis of COPD according to the perturbed metabolic pathways. Metabolomic researches have indicated that the dysfunctions of amino acid metabolism, lipid metabolism, energy production pathways, and the imbalance of oxidations and antioxidations might lead to local and systematic inflammation by activating the Nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway and releasing inflammatory cytokines, like interleutin-6 (IL-6), tumor necrosis factor-α, and IL-8. In addition, they might cause protein malnutrition and oxidative stress and contribute to the development and exacerbation of COPD.

An Updated Overview of Metabolomic Profile Changes in Chronic Obstructive Pulmonary Disease.

A specific gut microbiota and metabolomic profiles shifts related to antidiabetic action: The similar and complementary antidiabetic properties of type 3 resistant starch from Canna edulis and metformin.

Background Chronic obstructive pulmonary disease (COPD) is a common disease characterized by persistent respiratory symptoms and airflow restriction. It is usually manifested as airway and/or alveolar abnormalities caused by significant exposure to harmful particulates or gases. Objective We aim to explore plasma metabolomic changes in the acute exacerbation stage of COPD (AECOPD) and stable stage of COPD (Stable COPD) to identify potential biomarkers for diagnosis or prognosis in clinical practice. Methods Untargeted metabolomics and lipidomics analyses were performed to investigate dysregulated molecules in blood plasma of AECOPD patients (n=48) and Stable COPD (n=48), and a cohort of healthy people were included as a control group (n=48). Statistical analysis and bioinformatics analysis were performed to reveal dysregulated metabolites and perturbed metabolic pathways. SVM-based multivariate ROC analysis was used for candidate biomarker screening. Results A total of 142 metabolites and 688 lipids were dysregulated in COPD patients. Pathway enrichment analysis showed that several metabolic pathways were perturbed after COPD onset. Several biomarker panels were proposed for diagnosis of COPD vs healthy control and AECOPD vs Stable COPD with AUC greater than 0.9. Conclusion Numerous plasma metabolites and several metabolic pathways were detected relevant to COPD disease onset or progression. These metabolites may be considered as candidate biomarkers for diagnosis or prognosis of COPD. The perturbed pathways involved in COPD provide clues for further pathological mechanism studies of COPD.

/pdf/plasma-metabolomics-and-lipidomics-reveal-perturbed-5amc3ytp2b.pdf

Plasma Metabolomics and Lipidomics Reveal Perturbed Metabolites in Different Disease Stages of Chronic Obstructive Pulmonary Disease.

There are numerous prescription drugs and non-prescription drugs that cause drug-induced liver injury (DILI), which is the main cause of liver disease in humans around the globe. Its mechanism becomes clearer as the disease is studied further. For an instance, when acetaminophen (APAP) is taken in excess, it produces N-acetyl-p-benzoquinone imine (NAPQI) that binds to biomacromolecules in the liver causing liver injury. Treatment of DILI with traditional Chinese medicine (TCM) has shown to be effective. For example, activation of the Nrf2 signaling pathway as well as regulation of glutathione (GSH) synthesis, coupling, and excretion are the mechanisms by which ginsenoside Rg1 (Rg1) treats APAP-induced acute liver injury. Nevertheless, reducing the toxicity of TCM in treating DILI is still a problem to be overcome at present and in the future. Accumulated evidences show that hydrogel-based nanocomposite may be an excellent carrier for TCM. Therefore, we reviewed TCM with potential anti-DILI, focusing on the signaling pathway of these drugs' anti-DILI effect, as well as the possibility and prospect of treating DILI by TCM based on hydrogel materials in the future. In conclusion, this review provides new insights to further explore TCM in the treatment of DILI. 

Progress in the treatment of drug-induced liver injury with natural products.

Intestinal-targeted nanotubes-in-microgels composite carriers for capsaicin delivery and their effect for alleviation of Salmonella induced enteritis.

In order to compare the effect of dexamethasone and bergenin on chronic bronchitis and to reveal their anti-inflammatory mechanisms, (1)H NMR-based metabolomics was performed to explore the potential biomarkers of the disease and study the therapeutic mechanisms of the drugs. In this study, 40 Sprague-Dawley male rats were randomly divided into 4 groups, namely control, model, dexamethasone and bergenin groups, with 10 rats in each group. Except for the control group, rats from the other three groups were exposed to tobacco smoke for 1 h d(-1) for 28 days. During the modeling, dexamethasone (0.2 mg kg(-1)) and bergenin (87 mg kg(-1)) were administered orally to dexamethasone or bergenin rats 3 h after exposure every day. On the other hand, control and model rats were intragastrically administered water. According to the results of morphometric analysis of the airway epithelium and the count of white blood cells in the bronchoalveolar lavage fluid (BALF), dexamethasone and bergenin could suppress the infiltration of inflammatory cells, inhibit the secretion of mucus, and reduce white blood cells in BALF. Serum samples from the rats' orbits were collected every week. The metabolic profiles of sera were analyzed by multivariate statistical analyses, including PCA, PLS-DA and OPLS-DA models, and 18 metabolites were identified. The dynamic fluctuations of these biomarkers in sera from different groups were detected. The results suggested that the anti-inflammatory mechanism of dexamethasone may be associated with BCAA metabolism and glycolysis while bergenin could change BCAA metabolism, glycine, serine and threonine metabolism, and glycolysis to treat chronic bronchitis.

Comparative effects of dexamethasone and bergenin on chronic bronchitis and their anti-inflammatory mechanisms based on NMR metabolomics.

Tobacco smoke (TS) is a major causative agent to lead to chronic bronchitis (CB). However the mechanisms of CB induced by TS are unclear. In this report, rats were exposed to different concentrations of TS and the metabolic features of CB were characterized by using a nontargeted metabolic profiling method based on liquid chromatography-mass spectrometry (LC-MS) to detect the altered metabolic patterns in serum from CB rats and investigate the mechanisms of CB. 11 potential biomarkers were identified in serum of rats. Among them, the levels of lysophosphatidylethanolamine (18:1), lysophosphatidic acid (18:1), lysophosphatidylethanolamine (18:0), lysophosphatidylethanolamine (16:0), lysophosphatidylethanolamine (20:4), docosahexaenoic acid, 5-hydroxyindoleacetic acid and 5'-carboxy-γ-tocopherol were higher in TS group compared to control group. Conversely, the levels of 4-imidazolone-5-propionic acid, 12-hydroxyeicosatetraenoic acid and uridine were lower in TS group. The results indicated that the mechanism of CB was related to amino acid metabolism and lipid metabolism, particularly lipid metabolism. In addition, lysophosphatidylethanolamines were proved to be important mediators, which could be used as biomarkers to diagnose CB. These results also suggested that metabolomics was suitable for diagnosing CB and elucidating the possible metabolic pathways of TS-induced CB.

LC-MS based metabolomics identification of novel biomarkers of tobacco smoke-induced chronic bronchitis.

Tandem mass tags labeled quantitative proteomics to study the effect of tobacco smoke exposure on the rat lung.

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Intestinal-targeted nanotubes-in-microgels composite carriers for capsaicin delivery and their effect for alleviation of Salmonella induced enteritis.

Comparative effects of dexamethasone and bergenin on chronic bronchitis and their anti-inflammatory mechanisms based on NMR metabolomics.

LC-MS based metabolomics identification of novel biomarkers of tobacco smoke-induced chronic bronchitis.

Tandem mass tags labeled quantitative proteomics to study the effect of tobacco smoke exposure on the rat lung.