TY - JOUR

T1 - Short Term Exposure of Sheep Tracheal Epithelium to Cigarette Smoke Extract Reduces ENaC Current: A Pilot Study

AU - Jagirdar, Rajesh M.

AU - Grammatikopoulos, Alexandros

AU - Ioannou, Maria

AU - Solenov, Evgeniy

AU - Gourgoulianis, Konstantinos I.

AU - Hatzoglou, Chrissi

AU - Giannou, Anastasios D.

AU - Mercanoglou, Baris

AU - Zarogiannis, Sotirios G.

N1 - Copyright © 2024, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

PY - 2024/9/1

Y1 - 2024/9/1

N2 - Background/Aim: Cigarette smoke has been shown to induce a phenotype in humans known as “acquired cystic fibrosis”. This occurs because the cystic fibrosis transmembrane conductance regulator (CFTR) functions are impaired systemically due to the deleterious effects of smoke components. Elucidation of cigarette smoke effects on the tracheal epithelium is important. The aim of this study was to develop an ex vivo sheep tracheal model to investigate tracheal ion function. In this model, the epithelial sodium channel (ENaC) is inhibited after exposure to cigarette smoke extract (CSE) as a proof of principle. Materials and Methods: Tracheas were isolated from healthy sheep and the tracheal epithelium was surgically excised. Tissues were mounted in Ussing chambers and the short circuit current (Isc) was measured after incubation with 5% CSE in PBS or PBS alone for 30 min. The function of ENaC was investigated by the addition of amiloride (10–5M) apically. Western blot analysis was performed to assess differences in ENaC quantity after CSE exposure. Some specimens were stained with H&E for detection of histological alterations. Results: The amiloride effect on normal epithelium led to a significant decrease in Isc [ΔI=33±5.92 μA/cm2; p

AB - Background/Aim: Cigarette smoke has been shown to induce a phenotype in humans known as “acquired cystic fibrosis”. This occurs because the cystic fibrosis transmembrane conductance regulator (CFTR) functions are impaired systemically due to the deleterious effects of smoke components. Elucidation of cigarette smoke effects on the tracheal epithelium is important. The aim of this study was to develop an ex vivo sheep tracheal model to investigate tracheal ion function. In this model, the epithelial sodium channel (ENaC) is inhibited after exposure to cigarette smoke extract (CSE) as a proof of principle. Materials and Methods: Tracheas were isolated from healthy sheep and the tracheal epithelium was surgically excised. Tissues were mounted in Ussing chambers and the short circuit current (Isc) was measured after incubation with 5% CSE in PBS or PBS alone for 30 min. The function of ENaC was investigated by the addition of amiloride (10–5M) apically. Western blot analysis was performed to assess differences in ENaC quantity after CSE exposure. Some specimens were stained with H&E for detection of histological alterations. Results: The amiloride effect on normal epithelium led to a significant decrease in Isc [ΔI=33±5.92 μA/cm2; p

KW - Amiloride

KW - Ussing system

KW - cigarette smoke extract

KW - electrophysiology

KW - epithelial sodium channel

KW - tracheal epithelium

KW - Animals

KW - Epithelial Sodium Channels/metabolism

KW - Sheep

KW - Trachea/metabolism

KW - Pilot Projects

KW - Smoke/adverse effects

KW - Amiloride/pharmacology

KW - Respiratory Mucosa/metabolism

KW - Epithelium/drug effects

UR - https://www.scopus.com/record/display.uri?eid=2-s2.0-85202569690&origin=inward&txGid=b568dfb28271b1d6f7da0b8a73fb8138

UR - https://www.mendeley.com/catalogue/4bdbf07e-fa82-3da5-b642-6245763f0f9f/

U2 - 10.21873/invivo.13694

DO - 10.21873/invivo.13694

M3 - Article

C2 - 39187341

VL - 38

SP - 2294

EP - 2299

JO - In Vivo

JF - In Vivo

SN - 0258-851X

IS - 5

ER -