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Related Experiment Video

Updated: Jun 21, 2026

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Advanced 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

[Inflammatory cells and their mediators in COPD pathogenesis].

Cláudia Henrique da Costa¹, Rogério Rufino, José Roberto Lapa E Silva

¹Faculdade de Ciências Médicas, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ. ccosta@uerj.br

Revista Da Associacao Medica Brasileira (1992)

|July 25, 2009

Summary

Chronic Obstructive Pulmonary Disease (COPD) is a progressive lung disease. Understanding inflammatory cell recruitment is key to developing new COPD treatments that slow disease progression.

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Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment

Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment

Published on: June 24, 2020

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Last Updated: Jun 21, 2026

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Advanced 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

Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment

Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment

Published on: June 24, 2020

Area of Science:

Pulmonary Medicine
Immunology
Pathophysiology

Context:

Chronic Obstructive Pulmonary Disease (COPD) is a leading cause of mortality, characterized by progressive airflow obstruction and chronic inflammation, primarily due to tobacco smoking.
Current therapies do not halt COPD progression, highlighting the need for novel treatment strategies.
The pathogenesis involves structural changes in small airways driven by inflammatory cells like macrophages, neutrophils, and T cells.

Purpose:

To investigate the role of inflammatory cell influx in COPD pathogenesis.
To explore the involvement of specific chemokines (e.g., CXCL9, CXCL10, CXCL11, CCL5) in recruiting T cells and monocytes to the lungs.
To identify potential therapeutic targets by understanding mononuclear cell recruitment mechanisms.

Summary:

Tobacco smoking induces chronic inflammation and structural changes in COPD airways.
Macrophages, neutrophils, T cells (especially CD8+), and their interactions are critical in COPD.
Chemokines mediate the recruitment of inflammatory cells, increasing their numbers in COPD lungs.

Impact:

Elucidating the mechanisms of inflammatory cell recruitment enhances understanding of COPD pathophysiology.
Identifying key mediators involved in cell recruitment offers new targets for therapeutic interventions.
Developing treatments that block inflammatory cell influx may slow or halt COPD progression.