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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Respir+Res
2020 ; 21
(1
): 154
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
E-cigarette-induced pulmonary inflammation and dysregulated repair are mediated
by nAChR ?7 receptor: role of nAChR ?7 in SARS-CoV-2 Covid-19 ACE2 receptor
regulation
#MMPMID32552811
Wang Q
; Sundar IK
; Li D
; Lucas JH
; Muthumalage T
; McDonough SR
; Rahman I
Respir Res
2020[Jun]; 21
(1
): 154
PMID32552811
show ga
Electronic cigarette (e-cig) vaping is increasing rapidly in the United States,
as e-cigs are considered less harmful than combustible cigarettes. However,
limited research has been conducted to understand the possible mechanisms that
mediate toxicity and pulmonary health effects of e-cigs. We hypothesized that
sub-chronic e-cig exposure induces inflammatory response and dysregulated
repair/extracellular matrix (ECM) remodeling, which occur through the ?7
nicotinic acetylcholine receptor (nAChR?7). Adult wild-type (WT), nAChR?7
knockout (KO), and lung epithelial cell-specific KO (nAChR?7 CreCC10) mice were
exposed to e-cig aerosol containing propylene glycol (PG) with or without
nicotine. Bronchoalveolar lavage fluids (BALF) and lung tissues were collected to
determine e-cig induced inflammatory response and ECM remodeling, respectively.
Sub-chronic e-cig exposure with nicotine increased inflammatory cellular influx
of macrophages and T-lymphocytes including increased pro-inflammatory cytokines
in BALF and increased SARS-Cov-2 Covid-19 ACE2 receptor, whereas nAChR?7 KO mice
show reduced inflammatory responses associated with decreased ACE2 receptor.
Interestingly, matrix metalloproteinases (MMPs), such as MMP2, MMP8 and MMP9,
were altered both at the protein and mRNA transcript levels in female and male KO
mice, but WT mice exposed to PG alone showed a sex-dependent phenotype. Moreover,
MMP12 was increased significantly in male mice exposed to PG with or without
nicotine in a nAChR?7-dependent manner. Additionally, sub-chronic e-cig exposure
with or without nicotine altered the abundance of ECM proteins, such as collagen
and fibronectin, significantly in a sex-dependent manner, but without the direct
role of nAChR?7 gene. Overall, sub-chronic e-cig exposure with or without
nicotine affected lung inflammation and repair responses/ECM remodeling, which
were mediated by nAChR?7 in a sex-dependent manner.