Related Experiment Video
Updated: Sep 14, 2025
Noninvasive Sampling of Mucosal Lining Fluid for the Quantification of In Vivo Upper Airway Immune-mediator Levels
Published on: August 7, 2017
CXCL16/CXCR6 axis arises as a potential peripheral biomarker of early COPD development - results from a pilot study
Patrice Marques1,2,3, Irene Bocigas4, Elena Domingo1,2
1Department of Pharmacology, Faculty of Medicine and Odontology, University of Valencia, Valencia, Spain.
Background:
Chronic obstructive pulmonary disease (COPD) is mainly caused by long-term exposure to cigarette smoke. Since systemic inflammation is an important component of COPD pathophysiology, its characterization is essential for developing new biomarkers and pharmacological approaches. We have previously reported CXCL16/CXCR6 axis upregulation, a key element of leukocyte trafficking in COPD. Given the paucity of data on early-stage COPD patients (GOLD 1), we investigated CXCL16/CXCR6 axis expression in this population and in individuals at risk for developing COPD.
Design:
Blood samples were collected from 27 GOLD 1 patients, 27 symptomatic smokers with normal lung function (pre-COPD), and 14 non-smokers. CXCR6 expression was assessed in platelets, leukocytes, and leukocyte-platelet aggregates by flow cytometry. Plasma CXCL16 levels were measured by ELISA and lung function by spirometry.
Results:
CXCL16 plasma levels and CXCR6 expression on platelets, classical monocytes, B-cells, and leukocyte-platelet aggregates were higher in GOLD 1 patients than in non-smokers and pre-COPD subjects. While CXCR6 expression was similar between the pre-COPD group and non-smokers, plasma levels of CXCL16 were higher in the former. Finally, CXCL16/CXCR6 axis expression negatively correlated with FEV1/FVC ratio.
Conclusion:
This pilot study provides the first evidence that the CXCL16/CXCR6 axis is upregulated in early-COPD development. Increased CXCL16 plasma levels in GOLD 1 patients and pre-COPD subjects suggest CXCL16 as a potential peripheral biomarker of early COPD development. Given the importance of the CXCL16/CXCR6 axis in leukocyte trafficking, it may emerge as a druggable target to attenuate lung immune cell infiltration and prevent COPD development and progression.
More Related Videos
10:39Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
Published on: April 16, 2019
09:07Author Spotlight: Development and Characterization of an In Vitro Model to Study Chronic Cigarette Smoke Exposure and Its Impact on Airway Epithelial Cells in COPD Research
Published on: July 12, 2024
Related Concept Videos
01:20COPD: Pathogenesis and Clinical Features
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...
01:27Chronic Obstructive Pulmonary Disease-IV: Assessement and Diagnostic Studies
Medical History
01:20Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Inflammation
01:20Chronic Obstructive Pulmonary Disease-I: Introduction
01:22Chronic Obstructive Pulmonary Disease
Smoking is a primary risk factor for COPD, with over 80% of patients having a history of it. Patients typically experience progressive dyspnea or labored breathing, frequent coughing, and recurrent pulmonary infections. Many eventually succumb to respiratory failure, characterized by...