Table 1.
Roles of inflammasome in cigarette smoke-related diseases and physiopathological disorders.
| Reference | Year | Disease/disorder | Sample/Subjects | Effect of cigarette smoke on inflammasome |
|---|---|---|---|---|
| Mahalanobish et al. (21) | 2020 | COPD | Mouse lung tissue and BALF, human alveolar epithelial cells | Induce endoplasmic reticulum stress and mitochondrial dysfunctions, and further activate NLRP3 inflammasome |
| Rumora et al. (22) | 2020 | COPD | Human bronchial epithelial cells, monocyte-derived macrophages, and THP-1 cells | Increase NLRP3 and IL-1β |
| Rumora et al. (23) | 2021 | AECOPD | Human bronchial epithelial cells, monocyte-derived macrophages, and THP-1 cells | Increase NLRP3 and IL-1β |
| Ji et al. (24) | 2020 | AECOPD | Rat lung tissue and BALF, human bronchial epithelial cells | Increase caspase-1, NLRP3, IL-1β and IL-18 |
| Ozretic et al. (25) | 2019 | COPD | Human peripheral blood mononuclear and lung fibroblast cells | NLRP1 rs12150220 coding polymorphisms are associated with COPD disease severity |
| Nachmias et al. (26) | 2019 | COPD/AECOPD | Human alveolar epithelial cells | Increase NLRP3 and IL-1β |
| Wang et al. (27) | 2019 | COPD | Human bronchial and alveolar epithelial cells | Induce oxidative stress injury, promote Ca2+ influx, and increase caspase-1, NLRP3, IL-1β and IL-18 |
| Colarusso et al. (28) | 2019 | AECOPD | Human peripheral blood mononuclear cells | Increase AIM2/caspase-1/caspase-4 in IL-1α-induced TGF-β release |
| Cao et al. (29) | 2018 | COPD | Mouse lung tissue and BALF | Induce ROS production and increase NLRP3, cleaved-IL-1β and cleaved-caspase-1 |
| Wang et al. (30) | 2018 | AECOPD | Human peripheral blood mononuclear cells, bronchial tissues, serum and BALF | Increase NLRP3, caspase -1, ASC, IL-18 and IL-1β |
| Singh et al. (31) | 2018 | COPD | Human alveolar epithelial cells | Increase NLRP10, NLRP12, caspase-1, IL-1β, and IL-18 |
| Kaur et al. (32) | 2018 | COPD | Mouse lung tissue, human alveolar epithelial cells | Increase NLRP10, caspase-1, IL-1β, and IL-18 |
| Faner et al. (33) | 2016 | COPD/AECOPD | Human lung tissue of stable COPD, human sputum and plasma of AECOPD | Stable COPD: NLRP3 inflammasome is primed, but not activated; both caspase-1 and ASC were mostly inactive |
| Yang et al. (34) | 2016 | COPD | Mouse BALF | AECOPD: Caspase-1, oligomeric ASC, and associated cytokines (IL-1β, IL-18) were significantly increased |
| Di Stefano et al. (35) | 2014 | COPD | Human bronchial mucosa and BALF | Increase IL-1 and IL-18 |
| Rotta et al. (36) | 2013 | AECOPD | Mouse macrophage cells, human alveolar macrophages and human lung tissue | NLRP3 inflammasome is not activated in patients with stable COPD |
| Pauwels et al. (37) | 2011 | COPD | Mouse lung tissue | Increase NLRP3, caspase-1 and IL-1β |
| Mortaz et al. (38) | 2011 | COPD | Human bronchial epithelial cells | CS-induced inflammation occurred independently of IL-1β activation by the NLRP3/caspase-1 axis |
| Zhang et al. (39) | 2018 | ALI | Mouse lung tissue, mouse alveolar macrophages | Increase caspase-1 and IL-1β |
| Increase NLRP3, caspase-1 and IL-1β | ||||
| Mehta et al. (40) | 2020 | Atherosclerosis | Human THP-1 monocytes, macrophages, and foam cells | Activate MyD88/NF-κB pathway and increase NLRP3, caspase-1, IL-1β, and IL-18. |
| Wu et al. (41) | 2018 | Atherosclerosis | Mouse aortic tissue, human aortic endothelium cells | Induce ROS production and increase NLRP3, ASC, caspase-1, pro-caspase-1, IL-1β, and IL-18 |
| Yao et al. (42) | 2019 | Atherosclerosis | Rat vascular smooth muscle cells, rat aortic tissue | Induce ROS production and increase NLRP3 |
| Zheng et al. (43) | 2020 | Kidney injury | Mouse kidney tissue, human kidney cells | Induce NLRP6 inflammasome activation via alpha7 nicotinic acetylcholine receptor |
| Wu et al. (44) | 2020 | Bladder dysfunction | Human bladder tissue, human bladder urothelial cells | Induce oxidative stress injury and the activation of NLRP3 inflammasome |
| Buscetta et al. (45) | 2020 | Macrophage dysfunction | Human monocyte-derived macrophages and THP-1 cells | Inhibit NLRP3, caspase-1, IL-1β, and IL-18 acting mainly at the transcriptional level, and increase the caspase-1 activity via an NLRP3-independent and TLR4-TRIF-caspase-8-dependent pathway |
| Singh et al. (46) | 2019 | Podocyte injury | Mouse podocyte cells | Induce ROS production and increase the colocalization of NLRP3 with ASC, caspase-1 activity, and IL-1β production |
| Zhang et al. (47) | 2019 | Endothelial barrier dysfunction | Mouse microvascular endothelial cells and mouse coronary arterial endothelium | Increase HMGB1 and enhance cathepsin B-dependent NLRP3 inflammasome activation |
| Chen et al. (48) | 2019 | Endothelial barrier dysfunction | Human umbilical vein endothelial cells | Increase caspase-1, NLRP3, and IL-1β |
| Wang et al. (49) | 2019 | Endothelial dysfunction | Rat carotid artery tissue, human umbilical vein endothelial cells | Activate ROS/NLRP3 axis |
| Ye et al. (50) | 2019 | Oral leukoplakia | Rat oral mucosal epithelium | Reduce expression of the NLRP3 and diminish the secretion of IL-1β and IL-18 maturing by the NLRP3 inflammasome |
| Han et al. (51) | 2017 | Ubiquitin-mediated proteasomal processing | Human monocyte THP-1 cells and mouse lung tissue | Decrease NLRP3 protein abundance via increased ubiquitin-mediated proteasomal processing |
COPD, chronic obstructive pulmonary disease; BALF, bronchoalveolar lavage fluid; NLRP, nucleotide binding oligomerization domain and leucine, rich repeat containing receptor; IL, interleukin; AECOPD, acute exacerbation of chronic obstructive pulmonary disease; AIM, absent in melanoma; TGF, transforming growth factor; ASC, apoptosis associated speck like protein containing a caspase recruitment domain; TLR, Toll like receptor; TRIF, Toll/IL, 1receptor domain containing adaptor inducing interferon, beta; ROS, reactive oxygen species; HMGB1, high mobility group box 1.