2021
DOI: 10.3389/fimmu.2021.720049
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Roles of Inflammasome in Cigarette Smoke-Related Diseases and Physiopathological Disorders: Mechanisms and Therapeutic Opportunities

Abstract: Cigarette smoke damages a wide range of immunological functions, including innate and adaptive immune responses. Emerging literature demonstrates that inflammasome constitutes an essential component in innate immune response. In this review, we focus on the cumulative mechanisms of inflammasome in cigarette smoke-related diseases and physiopathological disorders, and summarize potential therapeutic opportunities targeting inflammasome. This review suggests that inflammasomes (NLRP3, NLRP6, NLRP12 and AIM2) are… Show more

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Cited by 18 publications
(14 citation statements)
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References 65 publications
(139 reference statements)
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“…Although other air pollutants have been shown to activate NLRP3 inflammasome and mediate pulmonary, cardiovascular, and neurodegenerative diseases (Saresella et al 2016 ; Zheng et al 2018 ; Du et al 2019 ), the effect of CS on the activation/inhibition of NLRP3 is still controversial and under debate. For instance, NLRP3 has been found to be negatively modulated by CS exposure in human THP1 cells and in mice (Han et al 2017 ; Buscetta et al 2020 ), whereas other studies indicate NLRP3 activation upon CS insult in bronchial epithelial cells and other pathologies as atherosclerosis, vascular and bladder dysfunctions, or brain injury (Li et al 2019 ; Mehta et al 2020 ; Rumora et al 2020 ; Wu et al 2020 ; Ma et al 2021 ). To our knowledge, the effect of CS on assembly and activation of skin inflammasome has never been described yet.…”
Section: Discussionmentioning
confidence: 99%
“…Although other air pollutants have been shown to activate NLRP3 inflammasome and mediate pulmonary, cardiovascular, and neurodegenerative diseases (Saresella et al 2016 ; Zheng et al 2018 ; Du et al 2019 ), the effect of CS on the activation/inhibition of NLRP3 is still controversial and under debate. For instance, NLRP3 has been found to be negatively modulated by CS exposure in human THP1 cells and in mice (Han et al 2017 ; Buscetta et al 2020 ), whereas other studies indicate NLRP3 activation upon CS insult in bronchial epithelial cells and other pathologies as atherosclerosis, vascular and bladder dysfunctions, or brain injury (Li et al 2019 ; Mehta et al 2020 ; Rumora et al 2020 ; Wu et al 2020 ; Ma et al 2021 ). To our knowledge, the effect of CS on assembly and activation of skin inflammasome has never been described yet.…”
Section: Discussionmentioning
confidence: 99%
“…The activation of these inflammasomes promotes pulmonary injury, contributing to the development of pulmonary fibrosis and inflammation [31]. However, other chemicals present in cigarette smoke, including nicotine and pollutants can also activate the NLRP3 inflammasome in human bronchial and alveolar epithelial cells [32][33][34].…”
Section: Inflammasomes In Lung Cancer Initiationmentioning
confidence: 99%
“…Arglabin inhibits the activation of NLRP3 inflammasome in macrophages, thus having an anti-inflammatory effect on atherosclerosis-prone mice by lowering serum levels of IL-1β [214]. NLRP3 inflammasomes are involved in cigarette-smoke-induced atherosclerosis [215]. Cigarette smoke activates NLRP3 inflammasome in monocytes, macrophages, and foam cells [216,217] Embolization of cholesterol crystals from atherosclerotic lesions of the major arteries causes the appearance of cholesterol-embolization syndrome, known as a systemic disease [218,219].…”
Section: Role Of Nlrp3 Inflammasome In Atherosclerosismentioning
confidence: 99%