Extrapulmonary effects of temporal exposure to cigarette smoke

Martins, Thais Lourenço; Campos, Keila Karine Duarte; Araújo, Natália Pereira da Silva; Machado, Dafne Fernandes; Bezerra, Frank Silva

doi:10.1177/0748233717715187

Cited by 6 publications

(6 citation statements)

References 45 publications

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“…Cigarette smoking is a crucial risk factor for cancers, respiratory, and cardiovascular diseases (Martins et al, 2017). Cigarette smoking is also an established risk factor for some oral diseases, such as periodontal disease, oral leukoplakia, and oral cancer (Wang et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Effects of active and passive smoking on salivary cytokines levels in rats: A pilot study

Guoyang

et al. 2018

Toxicol Ind Health

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Cigarette smoking is an established risk factor for some oral diseases. As an essential fluid in the oral cavity, saliva is crucial to maintain oral health. Relative to active smoking, there are very few studies assessing the effect of passive smoking on salivary cytokines levels. In the present study, we established the rat models by the means of the intraoral cigarette smoking or whole body cigarette smoke exposure to simulate human active or passive smoking, respectively. The effects of active or passive smoking on salivary cytokines levels were assessed by using ProcartaPlex multiplex immunoassays. The results of the current study indicated that both active and passive smoking diminished the body weights of rats and increased the levels of some blood counts. Intriguingly, active smoking enhanced the salivary levels of IL-6 and IL-12 p70 and passive smoking elevated the salivary IL-6 level. Moreover, active smoking appeared to have a more prominent activation effect on the salivary IL-6 level. It was noted that active or passive smoking had no significant effect on the salivary IFNlevel. Active or passive smoking could have potential effects on the salivary levels of some pro-inflammatory cytokines.

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Section: Introductionmentioning

confidence: 99%

Effects of active and passive smoking on salivary cytokines levels in rats: A pilot study

Guoyang

et al. 2018

Toxicol Ind Health

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“…Augmented levels of AST and gamma-GT were also observed in the untreated smoke-exposed group in our studies. Other research showed significant increase in biochemical parameters related to liver function, as serum levels of alanine aminotransferase (ALT), AST and total cholesterol were significantly higher in mice that were short-term exposed to cigarette smoke [39]. Moreover smokers with elevated blood pressure and serum gamma-GT levels are at higher risk of developing chronic kidney disease [49].…”

Section: Discussionmentioning

confidence: 99%

“…Studies have shown that levels of aspartate aminotransferase (AST), gamma glutamyl transferase (gamma-GT), glucose and cholesterol have been associated with cases of patients with exacerbated COPD [37][38][39][40]. Due to this we also investigated these biochemical parameters in the blood.…”

Section: Biochemical Blood Assaysmentioning

confidence: 99%

Mimetic peptide AC2-26 of annexin A1 as a potential therapeutic agent to treat COPD

Possebon

Costa

Souza

et al. 2018

International Immunopharmacology

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Chronic obstructive pulmonary disease (COPD) is related to inflammatory process caused by smoking habit. In this scenario, the anti-inflammatory protein Annexin A1 (AnxA1) may represent a therapeutic alternative. We performed experiments to evaluate the effects of the AnxA1 mimetic peptide Ac2-26 in an initial COPD model by physiological, histopathological, biochemical and immunohistochemical analyses. Weight loss, increased blood pressure, reductions in the pulmonary frequency and ventilation, loss of tracheal cilia, enlargement of the pulmonary intra-alveolar spaces and lymphoid tissue found in untreated smoke-exposed group were attenuated by AnxA1 peptide treatment. The Ac2-26 administration also protected against leukocytes influx in bronchoalveolar lavage (BAL), lung and trachea, and it also led to decreased hemoglobin, glucose, cholesterol, gamma glutamyl transferase and aspartato aminotransferase levels. Similarly, reduction of proinflammatory mediators and higher concentration of anti-inflammatory cytokine were found in macerated lung supernatant, blood plasma and BAL in the treated animals. Besides Ac2-26 group showed reduced tissue expressions of AnxA1, cyclooxygenase-2 and metalloproteinase-9, but formylated peptide receptor 2 (FPR2) overexpression. Our results all together highlighted the protective role of the Ac2-26 mimetic peptide in COPD with promising perspectives.

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“…After short-term exposure to CS for 5 days, the trachea and diaphragm of mice were infiltrated by inflammatory cells (Martins et al, 2017). Long-term CS exposure increases the risks of chronic obstructive pulmonary disease, lung cancer, and premature death (Nyunoya et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

“…CS inhalation has been reported to activate lung epithelial cell inflammation, cause DNA damage, and induce cell death ( Nyunoya et al, 2014 ). After short-term exposure to CS for 5 days, the trachea and diaphragm of mice were infiltrated by inflammatory cells ( Martins et al, 2017 ). Long-term CS exposure increases the risks of chronic obstructive pulmonary disease, lung cancer, and premature death ( Nyunoya et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Effects of Human Umbilical Cord-Derived Mesenchymal Stem Cells on the Acute Cigarette Smoke-Induced Pulmonary Inflammation Model

Chen

Lin

et al. 2020

Front. Physiol.

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Cigarette smoke (CS) has been reported to induce oxidative stress and inflammatory process in the lungs. However, the role of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) in the regulation of pulmonary inflammation remains unclear. The objective of this study is to investigate the effects of hUC-MSCs on lung inflammation in the acute CS-induced pulmonary inflammation animal model. Eightweek-old male C57BL/6 mice were intravenously administered 3 × 10 6 , 1 × 10 7 , and 3 × 10 7 cells/kg of hUC-MSCs as well as normal saline alone (control) after 3 days of CS exposure. Mice exposed to high-efficiency particulate air (HEPA)-filtered room air served as the CS control group. High-dose (3 × 10 7 cells/kg) hUC-MSC administration significantly decreased tumor necrosis factor (TNF)-α in the bronchoalveolar lavage fluid (BALF) of CS-exposed mice (p < 0.05). The chemokine (CXC motif) ligand 1/keratinocyte chemoattractant (CXCL1/KC) in BALF were significantly reduced by low-dose (3 × 10 6 cells/kg) and high-dose (3 × 10 7 cells/kg) hUC-MSC (p < 0.05). Medium-dose hUC-MSC administration decreased interleukin (IL)-1β in lung of mice, and TNF-α and caspase-3 were decreased in the lung of CS-exposed mice by mediumand high-dose MSC (p < 0.05). Low-dose hUC-MSCs significantly elevated serum CXCL1/KC and IL-1β in CS-exposed mice (p < 0.05). Our results suggest that highdose hUC-MSCs reduced pulmonary inflammation and had antiapoptotic effects in acute pulmonary inflammation.

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Extrapulmonary effects of temporal exposure to cigarette smoke

Cited by 6 publications

References 45 publications

Effects of active and passive smoking on salivary cytokines levels in rats: A pilot study

Effects of active and passive smoking on salivary cytokines levels in rats: A pilot study

Mimetic peptide AC2-26 of annexin A1 as a potential therapeutic agent to treat COPD

Effects of Human Umbilical Cord-Derived Mesenchymal Stem Cells on the Acute Cigarette Smoke-Induced Pulmonary Inflammation Model

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