Article
Immunology
Zhen Chen, Hao Wu, Weiyang Fan, Jiashuo Zhang, Yue Yao, Weiwei Su, Yonggang Wang, Peibo Li
Summary: Extracellular vesicles play a role in maintaining lung homeostasis in cigarette smoke-induced lung diseases. Previous studies have shown that cigarette smoke extract-treated extracellular vesicles promote macrophage polarization, leading to the development of inflammatory responses. This study found that naringenin and cigarette smoke extract co-treated extracellular vesicles significantly inhibit macrophage polarization and the secretion of inflammatory factors. Furthermore, naringenin downregulates miR-21-3p in extracellular vesicles, which targets the PTEN/AKT cascade in macrophages and suppresses M1 macrophage polarization. It also decreases PARP1 expression in extracellular vesicles, potentially suppressing M1 macrophage polarization. These findings provide new pharmacological references for naringenin in the treatment of cigarette smoke-induced lung inflammatory diseases.
FRONTIERS IN IMMUNOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Zhen Chen, Hao Wu, Rui Shi, Weiyang Fan, Jiashuo Zhang, Weiwei Su, Yonggang Wang, Peibo Li
Summary: Cigarette smoke-induced inflammation in the lungs, leading to conditions like COPD, is influenced by macrophage polarization and cross-talk between alveolar macrophages and lung epithelial cells via exosomes and miRNAs. This study identified differentially expressed exosomal miRNAs and their target genes involved in regulating macrophage polarization pathways. Furthermore, miR-21-3p and miR-27b-3p were found to play critical roles in promoting macrophage polarization in response to cigarette smoke exposure.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2021)
Article
Multidisciplinary Sciences
Shunsuke Yamaga, Keita Tanigaki, Eriko Nakamura, Naoko Sasaki, Yuta Kato, Masae Kuboniwa, Michiya Matsusaki, Atsuo Amano, Hiroki Takeuchi
Summary: The effects of cigarette smoke extract (CSE) on JAM1 and CXADR in human gingival epithelial cells were examined. CSE caused translocation of JAM1 to EGFR-positive endosomes, while CXADR did not. CSE increased permeability to lipopolysaccharide and peptidoglycan in a three-dimensional gingival tissue model, but overexpression of JAM1 prevented penetration by these substrates. Vitamin C increased JAM1 expression and inhibited penetration of LPS and PGN induced by CSE, indicating its protective effect on gingival barrier function.
SCIENTIFIC REPORTS
(2023)
Article
Dentistry, Oral Surgery & Medicine
Ayla Ozturk, Sevda Kurt-Bayrakdar, Bahattin Avci
Summary: The levels of hBD-2 in GCF were higher in patients with chronic periodontitis, while levels in serum were lower compared to healthy controls.
Article
Dentistry, Oral Surgery & Medicine
Mari Tatsumi, Manabu Yanagita, Motozo Yamashita, Shiori Hasegawa, Kuniko Ikegami, Masahiro Kitamura, Shinya Murakami
Summary: Long-term exposure to nicotine or cigarette smoke condensate (CSC) significantly suppresses cellular proliferation and migration of human gingival fibroblasts (HGFs), increases cellular senescence, and stimulates the inflammatory response. These negative effects may accelerate the progression of periodontal diseases.
JOURNAL OF PERIODONTAL RESEARCH
(2021)
Article
Dentistry, Oral Surgery & Medicine
Kubra Aral, Michael R. Milward, Paul R. Cooper
Summary: This study aimed to investigate the potential regulatory pathways of IL-1 beta production by monitoring the effects of periodontal pathogens Fn and Pg on inflammasomes and their regulators in HGFs. The results showed that Fn and Pg, especially when combined with ATP exposure, could dysregulate NLRP3, AIM2, IL-1 beta, ASC, and other inflammasome components and regulators, ultimately affecting the production of IL-1 beta.
Article
Medicine, Research & Experimental
Tingting Wu, Keye Xu, Chaobo Liu, Yan Li, Mingcai Li
Summary: This study aimed to investigate the effect of interleukin-37 (IL-37) on cigarette smoke-induced lung inflammation. By administering IL-37-expressing lentivirus to mice, it was found that IL-37 can alleviate weight loss and pulmonary inflammation induced by cigarette smoke. IL-37 also significantly inhibited inflammatory cell recruitment, reduced inflammatory cell increase, and suppressed the production of pro-inflammatory cytokines.
BIOMEDICINE & PHARMACOTHERAPY
(2022)
Article
Biochemistry & Molecular Biology
Cassio Luiz Coutinho Almeida-da-Silva, Harmony Matshik Dakafay, Kaitlyn Liu, David M. Ojcius
Summary: Evidence shows cigarette smoke has harmful effects on oral and systemic health. Recently, a link between smoking and susceptibility to COVID-19 was suggested. The study found cigarette smoke upregulates SARS-CoV-2 receptor expression and infection in oral cells, potentially leading to therapeutic interventions for preventing viral infection.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Immunology
Tiantian Cen, Yifeng Mai, Jie Jin, Minxuan Huang, Mingcai Li, Shanshan Wang, Hongying Ma
Summary: Our study aimed to investigate the ability of IL-41 to protect against CS-induced lung inflammation in vivo. The results showed that IL-41 pre-treatment alleviated pulmonary inflammatory infiltration and lung tissue lesions, limited CS-induced weight loss, and promoted the polarization of M2 macrophages. IL-41 also increased the levels of IL-10 and reduced the production of TNF-α, IL-6, and IL-1β.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Pengfei Zhang, Junbao Zhu, Linjie Zhang, Xiaolan Lv, Dongwei Guo, Lijun Liao, Shigao Huang, Zheng Peng
Summary: Objective of this study was to investigate the effects of Ginkgo biloba extract (GBE) on autophagy in human macrophages stimulated by cigarette smoke extract (CSE). Multiple experiments were conducted to observe the autophagy function of macrophages and the impact of GBE on it. The results showed that GBE could enhance the autophagy function of macrophages and reduce the damaging effect of CSE.
FRONTIERS IN BIOSCIENCE-LANDMARK
(2023)
Article
Multidisciplinary Sciences
Ashish Saxena, Matthew S. Walters, Jae-Hung Shieh, Ling-Bo Shen, Kazunori Gomi, Robert J. Downey, Ronald G. Crystal, Malcolm A. S. Moore
Summary: The airway basal cells communicate with endothelial cells through exosome-enriched EVs, promoting cell survival via VEGFR2 activation and involvement of VEGFA. However, downstream signaling pathways involved in airway basal cell EVs may be distinct from other signaling pathways.
SCIENTIFIC REPORTS
(2021)
Article
Environmental Sciences
Jung-Min Park, Haerin Jeong, Yoon-Seok Seo, Van Quan Do, Seong-Jin Choi, Kyuhong Lee, Kyung-Chul Choi, Won Jun Choi, Moo-Yeol Lee
Summary: The presence of bicarbonate in the experimental conditions influences the superoxide generation induced by cigarette smoke, with peroxidase treatment reducing more than half of the superoxide production. This suggests that peroxides and peroxy acids are the main contributors to superoxide production in this process.
Article
Medicine, Research & Experimental
Meng-Yu Zhang, Ying-Xiao Jiang, Yi-Can Yang, Jian-Yu Liu, Chen Huo, Xiu-Li Ji, Yi-Qing Qu
Summary: The study found that cigarette smoke induces inflammation and promotes pyroptosis in 16HBE cells through the ROS/NLRP3/caspase-1 pathway.
Article
Physiology
Qing Chen, Maaike de Vries, Kingsley Okechukwu Nwozor, Jacobien A. Noordhoek, Corry-Anke Brandsma, H. Marike Boezen, Irene H. Heijink
Summary: Our study found that the expression of FAM13A is lower in the airway epithelium of COPD patients compared to non-COPD controls, and cigarette smoke exposure selectively downregulates FAM13A expression in COPD patients. Overexpression of FAM13A significantly increases the rate of epithelial resistance establishment, accompanied by higher E-cadherin expression and reduced levels of CSE-induced CXCL8 secretion.
FRONTIERS IN PHYSIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Ignazio Restivo, Alessandro Attanzio, Ilenia Concetta Giardina, Francesca Di Gaudio, Luisa Tesoriere, Mario Allegra
Summary: Research shows that exposure to cigarette smoke can induce apoptosis in red blood cells, involving the initiation of DISC formation by p38 MAPK and activation of caspase-8/caspase-3 through ceramide generation.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)