High DHA tuna oil alleviated cigarette smoking exposure induced lung inflammation via the regulation of gut microbiota and serum metabolites

Bladder cancer is widely studied for its association with cigarette smoke (CS) exposure. Nicotine and carcinogenic substances in CS could induce chronic inflammatory state and DNA damage. This research was aimed to investigate the effect of CS exposure in chronic inflammatory state and p53 expression in bladder epithelial of Wistar rats. 25 male Wistar rats aged 6-8 weeks were divided into five groups as follows: Control (without treatment); CS-1, CS-2, CS-4, and CS-8 (treated with CS 1x, 2x, 4x, and 8x/day, respectively). Each exposure was done for 15 minutes for 60 days. Chronic inflammatory score was calculated from HE-stained specimens and Immunohistochemistry method was applied to measure p53 expression. Results showed that lymphocyte and histiocyte count in CS-8 was significantly higher as compared to CS-1 (p<0.05) and control (p<0.05). Lymphocyte and histiocyte count in CS-4 was also significantly higher compared to non-treated group (p<0.05). Chronic inflammatory score was significantly higher in CS-8 compared to other group (p<0.05). Moreover, p53 expression was found in CS-8 group (2 of 5 subjects had positive p53 expression, 20 positive cells in from total 10 hpf) and significantly different with other groups (p=0.011). Correlation study showed significant correlation between frequency of cigarette smoking exposure and lymphocyte count (p=0.000; r=0.956); monocyte count (p=0.000; r=0.928); chronic inflammation score (p=0.000; r=0.928); and p53 expression (p=0.007; r=0.522). We concluded that there was significant differences in chronic inflammation state and p53 expression among groups. Correlation study showed that frequency of cigarette smoking exposure was positively correlated with chronic inflammation and p53 expression.

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Cigarette Smoking Exposure Alters Pebp1 DNA Methylation and Protein Profile Involved in MAPK Signaling Pathway in Mice Testis1

Biology of Reproduction ◽

10.1095/biolreprod.113.111245 ◽

2013 ◽

Vol 89 (6) ◽

Cited By ~ 14

Author(s):

Wangjie Xu ◽

Peng Fang ◽

Zijue Zhu ◽

Jingbo Dai ◽

Dongsheng Nie ◽

...

Keyword(s):

Dna Methylation ◽

Cigarette Smoking ◽

Signaling Pathway ◽

Protein Profile ◽

Mapk Signaling ◽

Mapk Signaling Pathway ◽

Smoking Exposure ◽

Cigarette Smoking Exposure

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Effect of Smoke Exposure on Chronic Inflammation and P53 Expression in Pelvis Epithelial

International Journal of Innovative Technology and Exploring Engineering - Special Issue ◽

10.35940/ijitee.c1065.0193s20 ◽

2020 ◽

Vol 9 (3S) ◽

pp. 282-288

Keyword(s):

Cigarette Smoking ◽

Chronic Inflammation ◽

Lymphocyte Count ◽

Correlation Study ◽

Upper Urinary Tract ◽

Smoke Exposure ◽

Male Rats ◽

P53 Expression ◽

Smoking Exposure ◽

Cigarette Smoking Exposure

Many risk factors can cause upper urinary tract carcinoma. Smoking is the most influential risk factor and is associated with the formation of aromatic acids and could induce apoptotic cycle. This research was aimed to examine the effect of cigarete smoke exposure on inflammatory state and p53 expression in renal pelvis epithelial of wistar rats. As many as 25 male rats aged 6-8 weeks were divided into five groups as follows: Control (without treatment); CS-1, CS-2, CS-4, and CS-8 (treated with CS 1x, 2x, 4x, and 8x/day, respectively). Each exposure was done for 15 minutes for 60 days. histopathological changes were evaluated from HE-stained specimens and immunohistochemistry method was applied to measure p53 expressio neutrophile and lymphocyte count in CS-8 was significantly higher as compared to CS-1 (p<0.05) and control (p<0.05). p53 expression was found in the CS-8 (3 out of 5 subjects had positive p53 expression, with a total of 4-7 cells from 10 hpf). Correlation study showed significant correlation between frequency of cigarette smoking exposure and neutrophile count (p=0.000; r=-0.856); lymphocyte count (p=0.000; r=0.985); and p53 expression (p=0.000; 0.072). We concluded that there were significant differences in acute inflammation state, chronic inflammation state and p53 expression among groups. Correlation study showed that frequency of cigarette smoking exposure was positively correlated with lymphocyte count and p53 expression.

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Impacts of Cigarette Smoking Status on Metabolomic and Gut Microbiota Profile in Male Patients With Coronary Artery Disease: A Multi-Omics Study

Frontiers in Cardiovascular Medicine ◽

10.3389/fcvm.2021.766739 ◽

2021 ◽

Vol 8 ◽

Author(s):

Xiaomin Hu ◽

Yue Fan ◽

Hanyu Li ◽

Ruilin Zhou ◽

Xinyue Zhao ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Cigarette Smoking ◽

Gut Microbiota ◽

Smoking Status ◽

Rrna Gene ◽

Microbial Composition ◽

Serum Metabolites ◽

Artery Disease ◽

Never Smokers

Background: Cigarette smoking has been considered a modifiable risk factor for coronary artery disease (CAD). Changes in gut microbiota and microbe-derived metabolites have been shown to influence atherosclerotic pathogenesis. However, the effect of cigarette smoking on the gut microbiome and serum metabolites in CAD remains unclear.Method: We profiled the gut microbiota and serum metabolites of 113 male participants with diagnosed CAD including 46 current smokers, 34 former smokers, and 33 never smokers by 16S ribosomal RNA (rRNA) gene sequencing and untargeted metabolomics study. A follow-up study was conducted. PICRUSt2 was used for metagenomic functional prediction of important bacterial taxa.Results: In the analysis of the microbial composition, the current smokers were characterized with depleted Bifidobacterium catenulatum, Akkermansia muciniphila, and enriched Enterococcus faecium, Haemophilus parainfluenzae compared with the former and never smokers. In the untargeted serum metabolomic study, we observed and annotated 304 discriminant metabolites, uniquely including ceramides, acyl carnitines, and glycerophospholipids. Pathway analysis revealed a significantly changed sphingolipids metabolism related to cigarette smoking. However, the change of the majority of the discriminant metabolites is possibly reversible after smoking cessation. While performing PICRUSt2 metagenomic prediction, several key enzymes (wbpA, nadM) were identified to possibly explain the cross talk between gut microbiota and metabolomic changes associated with smoking. Moreover, the multi-omics analysis revealed that specific changes in bacterial taxa were associated with disease severity or outcomes by mediating metabolites such as glycerophospholipids.Conclusions: Our results indicated that both the gut microbiota composition and metabolomic profile of current smokers are different from that of never smokers. The present study may provide new insights into understanding the heterogenic influences of cigarette smoking on atherosclerotic pathogenesis by modulating gut microbiota as well as circulating metabolites.

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