Related Experiment Video

Updated: Aug 8, 2025

Methods to Evaluate Cytotoxicity and Immunosuppression of Combustible Tobacco Product Preparations
09:25

Methods to Evaluate Cytotoxicity and Immunosuppression of Combustible Tobacco Product Preparations

Published on: January 10, 2015

11.5K

The role of transforming growth factor-β2 in cigarette smoke-induced lung inflammation and injury

Hsin-Kuo Ko1, Yi-Han Hsiao2, Mei-Jy Jeng3

  • 1Department of Chest Medicine, Taipei Veterans General Hospital, Taipei 11217, Taiwan, ROC; College of Medicine, National Yang Ming Chiao Tung University, Taipei 11221, Taiwan, ROC.

Life Sciences
|March 4, 2023
PubMed
Abstract

Insights

Transforming growth factor-β2 (TGF-β2) reduces inflammation and injury caused by cigarette smoke (CS) in the lungs. This study reveals TGF-β2

Area of Science:

  • Pulmonary Medicine
  • Cellular and Molecular Biology
  • Immunology

Background:

  • Transforming growth factor-β2 (TGF-β2) is implicated in chronic obstructive lung disease pathogenesis.
  • The specific role of TGF-β2 in cigarette smoke (CS)-induced lung inflammation and injury remains unelucidated.

Purpose of the Study:

  • To investigate the role of TGF-β2 in regulating CS-induced lung inflammation and injury.
  • To elucidate the underlying molecular mechanisms of TGF-β2's action in the lungs.

Main Methods:

  • Primary bronchial epithelial cells (PBECs) were treated with cigarette smoke extract (CSE) to assess TGF-β2 signaling.
  • Mice were exposed to CS and treated with TGF-β2 (intraperitoneal) or TGF-β2-containing whey protein extract (oral).
  • Lung inflammation and injury markers were analyzed in vitro and in vivo.

Main Results:

  • In vitro, TGF-β2 attenuated CSE-induced IL-8 production in PBECs via TGF-β receptor I (TGF-βRI), Smad3, and MAPK pathways.
  • In vivo, CS exposure led to increased bronchoalveolar lavage fluid protein, inflammatory cells, and MCP-1, indicating lung inflammation/injury.
  • TGF-β2 administration significantly reduced CS-induced lung inflammation and injury in mice.

Conclusions:

  • TGF-β2 mitigates CS-induced IL-8 production and lung inflammation/injury through the Smad3 signaling pathway.
  • TGF-β2 demonstrates potential as a therapeutic agent for CS-induced lung conditions.
  • Further clinical studies are warranted to explore the anti-inflammatory effects of TGF-β2 in human CS-induced lung inflammation.
Keywords:
Cigarette smokeLung epithelial cellLung inflammationSignaling pathwaySmad 3TGF-β2

More Related Videos

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition06:12

Using Nicotine in a Silica-Exposed Mouse Model to Promote Lung Epithelial-Mesenchymal Transition

Published on: March 3, 2023

844
Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System06:07

Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System

Published on: October 22, 2020

6.7K

Related Concept Videos

TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.5K
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
2.9K
COPD: Pathogenesis and Clinical Features01:20

COPD: Pathogenesis and Clinical Features

Chronic obstructive pulmonary disease (COPD) is a group of lung conditions that progressively worsen over time, including chronic bronchitis and emphysema. This cluster of diseases collectively leads to a gradual and irreversible decline in lung function over time.
The primary cause for the onset of COPD is cigarette smoking and exposure to air pollution. These hazardous factors initiate a chain reaction within the lungs, resulting in chronic inflammation, damage to the airways, and a...
406