Nicotinic acetylcholine receptors (nAChRs) are ligand-gated (cation-permeable) 68 proteins expressed in the brain and in non-neuronal cells including lung AEC, macrophages, In the lung, acetylcholine binding to nAChR leads to an allosteric conformational 82 change permitting the channel opening, followed by ion fluxes that participate in cell survival, 83 differentiation, and proliferation [14, 15] . Nicotine, one of the components of cigarette smoke, 84 acts as an agonist implicated in the inhibition of apoptosis and oxidative stress responses 85 ultimately leading to lung impairments due to long-term exposure [5, 16, 17] . Previous studies 86 have established that multiple single nucleotide nAChR polymorphisms are respectively 87 associated with risks of lung cancer and chronic obstructive pulmonary disease (COPD), 88 highlighting their potential implication in respiratory diseases [14, 18, 19 ]. In addition, it has 89 been hypothesized that the nAChRs may play a role in coronavirus disease 2019 (COVID-19) 90 and might represent a therapeutic target, particularly regarding their potential contribution in The data are expressed as mean values and percentages. Differences between groups were 183 determined using the Student t test. A p-value <0.05 was considered significant. 
Smoking-associated pulmonary nAChRs subunits transcripts expressions 188 Considering the whole lung containing all types of tissues (Figure 1A) , the 16 nAChRs were 189 detected among non-smoker subjects except for CHRNA7, that was consistent in both 190 datasets containing non-smokers ( Figure 1B) . CHRNB1/E were very highly expressed; identity with regard to cross-reactivity (Supplemental Table S2 and S3, Supplemental 230 Figure S1 ). We focussed here on bronchi and large bronchioles as well as smooth muscle and 231 blood vessels on FFPE tissues (Figure 5A and B) . CHRNA1/A2/A4/B3/G were not detected. 