The role of cigarette smoke-induced epigenetic alterations in inflammation

Zong, Dandan; Liu, Xiangming; Li, Jinhua; Ouyang, Ruoyun; Chen, Ping

doi:10.1186/s13072-019-0311-8

Cited by 125 publications

(76 citation statements)

References 203 publications

(256 reference statements)

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“…Cigarette smoking is a leading cause of chronic diseases, mainly through inflammation. 1 Cigarette smoke contains many toxicants and is associated with adverse health effects, primarily chronic obstructive pulmonary disease (COPD) and other systemic disease, heart disease, and cancer. 2 It is also a major risk factor for oral health concerns including periodontal diseases and is associated with increased dental implant failures.…”

Section: Introductionmentioning

confidence: 99%

Inflammatory biomarkers and growth factors in saliva and gingival crevicular fluid of e‐cigarette users, cigarette smokers, and dual smokers: A pilot study

Gajendra

Lawyer

et al. 2020

Journal of Periodontology

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Background: Cigarette smoking remains one of the leading public health threats worldwide. Electronic cigarettes (e-cigs) provide an alternative to conventional cigarette smoking; however, the evidence base of risks and benefits of e-cig use is new and growing. In this cross-sectional pilot study, the effect of e-cig use on biological profiles in saliva and gingival crevicular fluid (GCF) was assessed and compared with the profiles of cigarette smokers (CS), dual users, and non-users. The systemic inflammatory mediators between e-cig users (EC) and these other groups were also assessed. Methods: This pilot cross-sectional study recruited volunteer participants consisting of four groups, non-smokers (NS), CS, EC, and dual EC and cigarette smokers (DS). Saliva and GCF samples were collected and analyzed for biomarkers of inflammation, oxidative stress, anti-inflammatory lipid mediators, tissue injury and repair, and growth factors with immunoassay (enzyme-linked immunosorbent assay and Luminex). Results: Smoking status was confirmed via salivary cotinine. Prostaglandin E2 level was significantly increased in CS compared with EC and DS, but not significantly different in EC and DS groups compared with non-smokers (NS). Statistically significant differences were observed between groups of EC and NS (myeloperoxidase [MPO], matrix metalloproteinase-9) as well as between DS and EC for biomarkers of inflammatory mediators (receptor for advanced glycation end products [RAGE], MPO, uteroglobin/CC-10); between groups of DS and NS for extracellular newly identified RAGE binding protein and between CS and NS for MPO. No statistically significant differences in biomarkers of immunity (S100A8, S100A9, galectin-3), tissue injury and repair (Serpine1/PAI-1) and growth factors (brain-derived neurotrophic 1274

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Section: Introductionmentioning

confidence: 99%

Inflammatory biomarkers and growth factors in saliva and gingival crevicular fluid of e‐cigarette users, cigarette smokers, and dual smokers: A pilot study

Gajendra

Lawyer

et al. 2020

Journal of Periodontology

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“…Cigarette smoking can cause inflammation in many tissues 13–16 . The effects of smoking on the bladder are complex and unclear.…”

Section: Introductionmentioning

confidence: 99%

“…Cigarette smoking can cause inflammation in many tissues. [13][14][15][16] The effects of smoking on the bladder are complex and unclear. To date, accumulated evidence has shown there is a clear link between smoking and bladder cancer, and smoking can affect gene expression and induce local inflammation of bladder.…”

mentioning

confidence: 99%

Cigarette smoke induces the pyroptosis of urothelial cells through ROS/NLRP3/caspase‐1 signaling pathway

Liu

Zhu

et al. 2020

Neurourology and Urodynamics

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Aims: Cell death and inflammation are involved in the development of bladder dysfunction. Pyroptosis is programmed cell death, causing cytotoxic effects and local inflammation. As one of the biggest health threats in the world, smoking is also closely related to urinary system diseases. The aims of this study were to investigate the role of NLRP3 inflammasome-mediated pyroptosis in the bladder after cigarette smoke exposure. Methods: The expression of NLRP3 inflammasome and the activity of caspase-1 in bladder tissue was investigated after cigarette smoke exposure. In vitro, bladder urothelial cells were stimulated by cigarette smoke extract and then the activity of caspase-1 and the expression of NLRP3 inflammasome were measured. The role of oxidative stress was also assessed.

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“…Due to maternal smoking, for instance, it has been seen that DNA methylation at specific CpG sites of sorted cord blood CD4+ cells of their newborns can be altered, with hundreds of differentially methylated regions resulting overrepresented in vital regulatory units. In addition, cigarette smoke could also cause miRNA modifications in the human placenta, possibly altering embryonic gene expression [81]. This issue has not been discussed here because at our knowledge there are no available studies in existing literature reporting smoking exposure-induced epigenetic modifications in granulosa cells.…”

Section: Resultsmentioning

confidence: 99%

Looking Inside the World of Granulosa Cells: The Noxious Effects of Cigarette Smoke

2020

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The detrimental implications of tobacco smoke on systemic health have been widely established during the past few decades. Nonetheless, increasing evidence has begun to shed more light on the serious impact that smoke exposure could also have on mammal reproductive health in terms of overall ovarian dysfunction and gestation. A variety of these complications seem to be causally related to specific chemical substances contained in cigarette smoke and their possible effects on ovarian tissues and cells, such as granulosa cells. Granulosa cells represent the functional unit of the ovary and are able to establish a bidirectional cross-talk relationship with the oocyte during folliculogenesis, which makes them vital for its correct growth and development. Based on these premises, the current review focuses on the presence of related smoke-induced damages in granulosa cells. Data have been grouped according to the studied tobacco constituents and the molecular pathways involved, in order to synthesize their impact on granulosa cells and fertility. Attention is further brought to the correlation between electronic cigarettes and female reproduction, although there have been no investigations so far regarding e-cigarette-related granulosa cell exposure. We summarize how tobacco constituents are able to cause alterations in the “life” of granulosa cells, ranging from luteal steroidogenesis and follicular loss to granulosa cell apoptosis and activation of the autophagic machinery. Further studies have been conducted to elucidate the relationship between lifestyle and fertility as to reduce the morbidity connected with infertility.

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The role of cigarette smoke-induced epigenetic alterations in inflammation

Cited by 125 publications

References 203 publications

Inflammatory biomarkers and growth factors in saliva and gingival crevicular fluid of e‐cigarette users, cigarette smokers, and dual smokers: A pilot study

Inflammatory biomarkers and growth factors in saliva and gingival crevicular fluid of e‐cigarette users, cigarette smokers, and dual smokers: A pilot study

Cigarette smoke induces the pyroptosis of urothelial cells through ROS/NLRP3/caspase‐1 signaling pathway

Looking Inside the World of Granulosa Cells: The Noxious Effects of Cigarette Smoke

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