Related Experiment Video

Updated: May 3, 2026

Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment
09:00

Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment

Published on: June 24, 2020

3.0K

CXCL5-secreting pulmonary epithelial cells drive destructive neutrophilic inflammation in tuberculosis

Geraldine Nouailles, Anca Dorhoi, Markus Koch

    The Journal of Clinical Investigation
    |February 11, 2014
    PubMed

    Insights

    Tuberculosis lung inflammation is driven by polymorphonuclear leukocytes (PMNs). Blocking CXCL5, a chemokine, reduces PMN recruitment and inflammation, improving survival in mice with pulmonary tuberculosis.

    Area of Science:

    • Immunology
    • Pulmonary Medicine
    • Microbiology

    Background:

    • Host defense against pulmonary infections relies on polymorphonuclear leukocytes (PMNs) for bacterial clearance.
    • Excessive PMN accumulation can lead to severe lung injury.
    • The role of chemokines in PMN recruitment during Mycobacterium tuberculosis infection is not fully understood.

    Purpose of the Study:

    • To investigate the role of CXC chemokines, specifically CXCL5, in PMN recruitment during pulmonary tuberculosis.
    • To determine the impact of CXCL5 deficiency on host immune response and survival against M. tuberculosis.

    Main Methods:

    • Analysis of CXC chemokine gene expression in M. tuberculosis-infected murine lungs.
    • Generation and analysis of Cxcl5(-/-) and Cxcr2(-/-) knockout mice.
    • Assessment of PMN recruitment, bacterial clearance, inflammation, and survival following M. tuberculosis infection.

    Main Results:

    • M. tuberculosis infection upregulated Cxcr2 and its ligand Cxcl5 in murine lungs.
    • Cxcl5(-/-) and Cxcr2(-/-) mice showed enhanced survival against high-dose M. tuberculosis infection.
    • Resistance in Cxcl5(-/-) mice was attributed to reduced PMN recruitment and pulmonary inflammation, not improved bacterial clearance.
    • Lung epithelial cells were the primary source of CXCL5, with secretion dependent on TLR2 signaling.

    Conclusions:

    • TLR2-induced CXCL5 from lung epithelial cells is crucial for PMN-driven inflammation in pulmonary tuberculosis.
    • Targeting the CXCL5-CXCR2 axis may offer therapeutic strategies for tuberculosis by modulating destructive inflammation.

    More Related Videos

    Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy10:39

    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

    7.0K
    Fluorescence Assays for the Study of Mycobacterium tuberculosis Interaction with the Immune Receptor SLAMF107:42

    Fluorescence Assays for the Study of Mycobacterium tuberculosis Interaction with the Immune Receptor SLAMF1

    Published on: February 28, 2025

    1.1K

    Related Concept Videos

    Pulmonary Tuberculosis II01:28

    Pulmonary Tuberculosis II

    Tuberculosis, or TB, is a bacterial infectious disease caused by Mycobacterium tuberculosis. While its primary impact is on the lungs, leading to pulmonary tuberculosis, it can also affect various other organs, a condition referred to as extrapulmonary tuberculosis.
    Here is a detailed explanation of its pathophysiology:
    Transmission: The process begins when a person inhales droplet nuclei containing M. tuberculosis. These are typically released into the air when an individual with pulmonary or...
    2.5K
    Pulmonary Tuberculosis I01:29

    Pulmonary Tuberculosis I

    Tuberculosis, often called TB, is a contagious illness primarily caused by Mycobacterium tuberculosis. It mainly affects the lung parenchyma but can also impact other body parts.
    Causative Organism
    The primary infectious agent causing tuberculosis is Mycobacterium tuberculosis, a slow-growing, acid-fast, aerobic rod that exhibits sensitivity to heat and ultraviolet light. Instances of Mycobacterium bovis and Mycobacterium avium contributing to the development of TB infection are rare.
    Mode of...
    1.7K
    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
    5.0K
    Cystic Fibrosis: Pathogenesis01:23

    Cystic Fibrosis: Pathogenesis

    Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
    CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
    1.1K
    Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features01:24

    Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

    Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...
    40
    Inflammatory Bowel Disease III: Crohn's Disease01:25

    Inflammatory Bowel Disease III: Crohn's Disease

    Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
    35