scholarly journals Maternal Exposure to Secondhand Cigarette Smoke Primes the Lung for Induction of Phosphodiesterase-4D5 Isozyme and Exacerbated Th2 Responses: Rolipram Attenuates the Airway Hyperreactivity and Muscarinic Receptor Expression but Not Lung Inflammation and Atopy

2009 ◽  
Vol 183 (3) ◽  
pp. 2115-2121 ◽  
Author(s):  
Shashi P. Singh ◽  
Neerad C. Mishra ◽  
Jules Rir-sima-ah ◽  
Mathew Campen ◽  
Viswanath Kurup ◽  
...  
Keyword(s):  
Muscarinic Receptor ◽  
Cigarette Smoke ◽  
Lung Inflammation ◽  
Maternal Exposure ◽  
Airway Hyperreactivity ◽  
Receptor Expression ◽  
Th2 Responses

scholarly journals Cigarette Smoke Stimulates SARS-CoV-2 Internalization by Activating AhR and Increasing ACE2 Expression in Human Gingival Epithelial Cells

2021 ◽  
Vol 22 (14) ◽  
pp. 7669
Author(s):  
Cassio Luiz Coutinho Almeida-da-Silva ◽  
Harmony Matshik Dakafay ◽  
Kaitlyn Liu ◽  
David M. Ojcius
Keyword(s):  
Epithelial Cells ◽  
Oral Cavity ◽  
Cigarette Smoke ◽  
Large Body ◽  
Receptor Expression ◽  
Host Cells ◽  
Dependent Manner ◽  
Gingival Epithelial Cells ◽  
Human Gingival Epithelial Cells ◽  
Oral Cells

A large body of evidence shows the harmful effects of cigarette smoke to oral and systemic health. More recently, a link between smoking and susceptibility to coronavirus disease 2019 (COVID-19) was proposed. COVID-19 is due to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which uses the receptor ACE2 and the protease TMPRSS2 for entry into host cells, thereby infecting cells of the respiratory tract and the oral cavity. Here, we examined the effects of cigarette smoke on the expression of SARS-CoV-2 receptors and infection in human gingival epithelial cells (GECs). We found that cigarette smoke condensates (CSC) upregulated ACE2 and TMPRSS2 expression in GECs, and that CSC activated aryl hydrocarbon receptor (AhR) signaling in the oral cells. ACE2 was known to mediate SARS-CoV-2 internalization, and we demonstrate that CSC treatment potentiated the internalization of SARS-CoV-2 pseudovirus in GECs in an AhR-dependent manner. AhR depletion using small interference RNA decreased SARS-CoV-2 pseudovirus internalization in CSC-treated GECs compared with control GECs. Our study reveals that cigarette smoke upregulates SARS-CoV-2 receptor expression and infection in oral cells. Understanding the mechanisms involved in SARS-CoV-2 infection in cells of the oral cavity may suggest therapeutic interventions for preventing viral infection and transmission.

Effects of intranasal azithromycin on features of cigarette smoke-induced lung inflammation

2021 ◽  
pp. 174467
Author(s):  
Siddhi Jain ◽  
Sneha Durugkar ◽  
Pritam Saha ◽  
Sharad B. Gokhale ◽  
V.G.M. Naidu ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Lung Inflammation

Histamine Upregulates Th1 and Downregulates Th2 Responses due to Different Patterns of Surface Histamine 1 and 2 Receptor Expression

2001 ◽  
Vol 124 (1-3) ◽  
pp. 190-192 ◽  
Author(s):  
M. Jutel ◽  
S. Klunker ◽  
M. Akdis ◽  
J. Małolepszy ◽  
Oliver A.R. Thomet ◽  
...  
Keyword(s):  
Receptor Expression ◽  
Th2 Responses

scholarly journals p53- and PAI-1-mediated induction of C-X-C chemokines and CXCR2: importance in pulmonary inflammation due to cigarette smoke exposure

2016 ◽  
Vol 310 (6) ◽  
pp. L496-L506 ◽  
Author(s):  
Nivedita Tiwari ◽  
Amarnath S. Marudamuthu ◽  
Yoshikazu Tsukasaki ◽  
Mitsuo Ikebe ◽  
Jian Fu ◽  
...  
Keyword(s):  
Lung Injury ◽  
Cigarette Smoke ◽  
Lung Inflammation ◽  
Cellular Adhesion ◽  
Alveolar Epithelial Cells ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
P53 Expression ◽  
Cellular Adhesion Molecule ◽  
Pai 1

We previously demonstrated that tumor suppressor protein p53 augments plasminogen activator inhibitor-1 (PAI-1) expression in alveolar epithelial cells (AECs) during chronic cigarette smoke (CS) exposure-induced lung injury. Chronic lung inflammation with elevated p53 and PAI-1 expression in AECs and increased susceptibility to and exacerbation of respiratory infections are all associated with chronic obstructive pulmonary disease (COPD). We recently demonstrated that preventing p53 from binding to the endogenous PAI-1 mRNA in AECs by either suppressing p53 expression or blockading p53 interactions with the PAI-1 mRNA mitigates apoptosis and lung injury. Within this context, we now show increased expression of the C-X-C chemokines (CXCL1 and CXCL2) and their receptor CXCR2, and the intercellular cellular adhesion molecule-1 (ICAM-1), in the lung tissues of patients with COPD. We also found a similar increase in lung tissues and AECs from wild-type (WT) mice exposed to passive CS for 20 wk and in primary AECs treated with CS extract in vitro. Interestingly, passive CS exposure of mice lacking either p53 or PAI-1 expression resisted an increase in CXCL1, CXCL2, CXCR2, and ICAM-1. Furthermore, inhibition of p53-mediated induction of PAI-1 expression by treatment of WT mice exposed to passive CS with caveolin-1 scaffolding domain peptide reduced CXCL1, CXCL2, and CXCR2 levels and lung inflammation. Our study reveals that p53-mediated induction of PAI-1 expression due to chronic CS exposure exacerbates lung inflammation through elaboration of CXCL1, CXCL2, and CXCR2. We further provide evidence that targeting this pathway mitigates lung injury associated with chronic CS exposure.

scholarly journals Regulation of M3 Muscarinic Receptor Expression and Function by Transmembrane Protein 147

2010 ◽  
Vol 79 (2) ◽  
pp. 251-261 ◽  
Author(s):  
Erica Rosemond ◽  
Mario Rossi ◽  
Sara M. McMillin ◽  
Marco Scarselli ◽  
Julie G. Donaldson ◽  
...  
Keyword(s):  
Muscarinic Receptor ◽  
Transmembrane Protein ◽  
Receptor Expression ◽  
And Function ◽  
M3 Muscarinic Receptor

scholarly journals Early Detection of Susceptibility to Acute Lung Inflammation by Molecular Imaging in Mice Exposed to Cigarette Smoke

2011 ◽  
Vol 10 (5) ◽  
pp. 7290.2011.00010 ◽  
Author(s):  
Sandra Pérez-Rial ◽  
Laura del Puerto-Nevado ◽  
Nicolás González-Mangado ◽  
Germán Peces-Barba
Keyword(s):  
Molecular Imaging ◽  
Early Detection ◽  
Cigarette Smoke ◽  
Lung Inflammation ◽  
Acute Lung Inflammation

scholarly journals Genetic Ablation of NADPH Oxidase Enhances Susceptibility to Cigarette Smoke-Induced Lung Inflammation and Emphysema in Mice

2008 ◽  
Vol 172 (5) ◽  
pp. 1222-1237 ◽  
Author(s):  
Hongwei Yao ◽  
Indika Edirisinghe ◽  
Se-Ran Yang ◽  
Saravanan Rajendrasozhan ◽  
Aruna Kode ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Cigarette Smoke ◽  
Lung Inflammation ◽  
Genetic Ablation
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