Article ; Online: The activation of the AIM2 inflammasome after cigarette smoke exposure leads to an immunosuppressive lung microenvironment.
International immunopharmacology
2024 Volume 131, Page(s) 111832
Abstract: Cigarette smoke is widely known as contributing to chronic inflammation underlying several airway diseases, such as chronic obstructive pulmonary disease (COPD) and lung cancer. In our previous studies we found that the lung of both COPD and cancer ... ...
| Abstract | Cigarette smoke is widely known as contributing to chronic inflammation underlying several airway diseases, such as chronic obstructive pulmonary disease (COPD) and lung cancer. In our previous studies we found that the lung of both COPD and cancer patients were characterized by the presence and activation of the AIM2 inflammasome. Here, we wanted to investigate the upstream step during the establishment of chronic lung inflammation after cigarette smoke exposure. We took advantage of a mouse model of smoking exposure and public scRNAseq data. We found that AIM2 mRNA was expressed in both alveolar type II, B cells, T regulatory (Treg) and macrophages detected in the lung of non-smokers (n = 4) and smokers (n = 3). The activation of AIM2 in smoking mice by using PolydA:dT did not alter cigarette-smoke-induced alveoli enlargement and mucus production, rather it induced higher recruitment of immunosuppressive cells, such as non-active dendritic cells (DCs), Arginase I+ macrophages, myeloid-derived suppressor cells (MDSC) and Tregs. In addition, the inflammatory environment after AIM2 activation in smoking mice was characterized by higher levels of IL-1α, IL-1β, IL-33, TNFα, LDH, IL-10 and TGFβ. This scenario was not altered after the pharmacological inhibition of both caspase-1 and STING pathway. In conclusion, these data suggest that chronic inflammation after cigarette smoke exposure is associated with AIM2 activation, which could lead towards cigarette smoke-associated lung diseases. |
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| MeSH term(s) | Animals ; Humans ; Mice ; Cigarette Smoking/adverse effects ; DNA-Binding Proteins/genetics ; Inflammasomes/metabolism ; Inflammation ; Lung/metabolism ; Mice, Inbred C57BL ; Pulmonary Disease, Chronic Obstructive | |||||
| Chemical Substances | AIM2 protein, human ; DNA-Binding Proteins ; Inflammasomes | |||||
| Language | English | |||||
| Publishing date | 2024-03-10 | |||||
| Publishing country | Netherlands | |||||
| Document type | Journal Article | |||||
| ZDB-ID | 2043785-7 | |||||
| ISSN | 1878-1705 ; 1567-5769 | |||||
| ISSN (online) | 1878-1705 | |||||
| ISSN | 1567-5769 | |||||
| DOI | 10.1016/j.intimp.2024.111832 | |||||
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| Database | MEDical Literature Analysis and Retrieval System OnLINE |
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