Long-term smoking contributes to aging frailty and inflammatory response

In recent years, the health challenges linked to frailty in the elderly, particularly those worsened by cigarette smoke, have become more pronounced. However, quantitative studies examining the impact of smoking dosage on frailty in this population remain limited. To address this gap, we developed...

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Main Authors: Huijin Hou, Yidi Chai, Ting Zhang, Yue Liang, Lan Huang, Xu Cao, Shufang Liang
Format: Article
Language:English
Published: Association of Basic Medical Sciences of Federation of Bosnia and Herzegovina 2025-01-01
Series:Biomolecules & Biomedicine
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Online Access:https://www.bjbms.org/ojs/index.php/bjbms/article/view/11722
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author Huijin Hou
Yidi Chai
Ting Zhang
Yue Liang
Lan Huang
Xu Cao
Shufang Liang
author_facet Huijin Hou
Yidi Chai
Ting Zhang
Yue Liang
Lan Huang
Xu Cao
Shufang Liang
author_sort Huijin Hou
collection DOAJ
description In recent years, the health challenges linked to frailty in the elderly, particularly those worsened by cigarette smoke, have become more pronounced. However, quantitative studies examining the impact of smoking dosage on frailty in this population remain limited. To address this gap, we developed a model using smoke-exposed elderly mice. Fifteen-month-old C57BL/6J mice were exposed to smoke from two burning cigarettes for 15 minutes in a whole-body chamber. This exposure occurred 4, 6, and 8 times daily for 30 days, representing low, medium, and high smoking dosages, respectively. Frailty levels were assessed through rotation and grip strength tests, alongside lung histopathology and inflammatory factor protein expression analyses across the three dosage groups. Additionally, we used the GEO database to validate the correlation between frailty and inflammation in elderly smokers, facilitating cross-comparisons between animal model findings and human sample data. Our results show that mice exposed to high-dose smoking were significantly more prone to frailty, with notable reductions in maximal grip strength (p < 0.01) and drop time (p < 0.001). Among human samples, 69.2% of elderly smokers exhibited a frailty phenotype, compared to just 15.4% of non-smokers. Both smoking-exposed mice and elderly smokers demonstrated up-regulation of tumor necrosis factor- α (TNF-α) and interleukin-1 β (IL-1β) in lung tissue and serum. Mechanistically, this up-regulation activates the NF-κB signaling pathway. Our findings quantitatively link smoking-induced frailty to increased levels of TNF-α and IL-1β, providing experimental evidence for the diagnosis and prevention of frailty in elderly populations.
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spelling doaj-art-d8a3b4c0bf474396a3b1c43a3a9b020f2025-01-22T16:40:58ZengAssociation of Basic Medical Sciences of Federation of Bosnia and HerzegovinaBiomolecules & Biomedicine2831-08962831-090X2025-01-0110.17305/bb.2024.11722Long-term smoking contributes to aging frailty and inflammatory responseHuijin Hou0Yidi Chai1Ting Zhang2Yue Liang3Lan Huang4Xu Cao5Shufang Liang6China Tobacco Sichuan Industrial Co., Ltd., Chengdu, China; Harmful Components and Tar Reduction in Cigarette Key Laboratory of Sichuan Province, Chengdu, China; Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaChina Tobacco Sichuan Industrial Co., Ltd., Chengdu, China; Harmful Components and Tar Reduction in Cigarette Key Laboratory of Sichuan Province, Chengdu, ChinaChina Tobacco Sichuan Industrial Co., Ltd., Chengdu, China; Harmful Components and Tar Reduction in Cigarette Key Laboratory of Sichuan Province, Chengdu, ChinaChina Tobacco Sichuan Industrial Co., Ltd., Chengdu, China; Harmful Components and Tar Reduction in Cigarette Key Laboratory of Sichuan Province, Chengdu, China; Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaChina Tobacco Sichuan Industrial Co., Ltd., Chengdu, China; Harmful Components and Tar Reduction in Cigarette Key Laboratory of Sichuan Province, Chengdu, China; Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaChina Tobacco Sichuan Industrial Co., Ltd., Chengdu, China; Harmful Components and Tar Reduction in Cigarette Key Laboratory of Sichuan Province, Chengdu, China; Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaChina Tobacco Sichuan Industrial Co., Ltd., Chengdu, China; Harmful Components and Tar Reduction in Cigarette Key Laboratory of Sichuan Province, Chengdu, China; Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China In recent years, the health challenges linked to frailty in the elderly, particularly those worsened by cigarette smoke, have become more pronounced. However, quantitative studies examining the impact of smoking dosage on frailty in this population remain limited. To address this gap, we developed a model using smoke-exposed elderly mice. Fifteen-month-old C57BL/6J mice were exposed to smoke from two burning cigarettes for 15 minutes in a whole-body chamber. This exposure occurred 4, 6, and 8 times daily for 30 days, representing low, medium, and high smoking dosages, respectively. Frailty levels were assessed through rotation and grip strength tests, alongside lung histopathology and inflammatory factor protein expression analyses across the three dosage groups. Additionally, we used the GEO database to validate the correlation between frailty and inflammation in elderly smokers, facilitating cross-comparisons between animal model findings and human sample data. Our results show that mice exposed to high-dose smoking were significantly more prone to frailty, with notable reductions in maximal grip strength (p < 0.01) and drop time (p < 0.001). Among human samples, 69.2% of elderly smokers exhibited a frailty phenotype, compared to just 15.4% of non-smokers. Both smoking-exposed mice and elderly smokers demonstrated up-regulation of tumor necrosis factor- α (TNF-α) and interleukin-1 β (IL-1β) in lung tissue and serum. Mechanistically, this up-regulation activates the NF-κB signaling pathway. Our findings quantitatively link smoking-induced frailty to increased levels of TNF-α and IL-1β, providing experimental evidence for the diagnosis and prevention of frailty in elderly populations. https://www.bjbms.org/ojs/index.php/bjbms/article/view/11722Smokingfrailtytumor necrosis factor- αTNF-αinterleukin-1 βIL-1β
spellingShingle Huijin Hou
Yidi Chai
Ting Zhang
Yue Liang
Lan Huang
Xu Cao
Shufang Liang
Long-term smoking contributes to aging frailty and inflammatory response
Biomolecules & Biomedicine
Smoking
frailty
tumor necrosis factor- α
TNF-α
interleukin-1 β
IL-1β
title Long-term smoking contributes to aging frailty and inflammatory response
title_full Long-term smoking contributes to aging frailty and inflammatory response
title_fullStr Long-term smoking contributes to aging frailty and inflammatory response
title_full_unstemmed Long-term smoking contributes to aging frailty and inflammatory response
title_short Long-term smoking contributes to aging frailty and inflammatory response
title_sort long term smoking contributes to aging frailty and inflammatory response
topic Smoking
frailty
tumor necrosis factor- α
TNF-α
interleukin-1 β
IL-1β
url https://www.bjbms.org/ojs/index.php/bjbms/article/view/11722
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AT tingzhang longtermsmokingcontributestoagingfrailtyandinflammatoryresponse
AT yueliang longtermsmokingcontributestoagingfrailtyandinflammatoryresponse
AT lanhuang longtermsmokingcontributestoagingfrailtyandinflammatoryresponse
AT xucao longtermsmokingcontributestoagingfrailtyandinflammatoryresponse
AT shufangliang longtermsmokingcontributestoagingfrailtyandinflammatoryresponse