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Published on: February 28, 2025
Augmented chemokine levels and chemokine receptor expression on immune cells during pulmonary tuberculosis
Supriya Pokkali1, Sulochana D Das
1Department of Immunology, Tuberculosis Research Centre (ICMR), Chennai, India.
Insights
Mycobacterium tuberculosis infection alters immune mediators, affecting cell movement. This study reveals how specific chemokines and cytokines change, influencing immune cell trafficking in pulmonary tuberculosis patients.
Area of Science:
- Immunology
- Infectious Diseases
- Molecular Biology
Background:
- Mycobacterium tuberculosis (M. tuberculosis) infection causes systemic immune changes.
- Cytokines and chemokines are key mediators of immune cell trafficking.
- Understanding these interactions is crucial for managing pulmonary tuberculosis (PTB).
Purpose of the Study:
- To investigate systemic changes in immune mediators during PTB.
- To analyze the synchronized interaction of cytokines and chemokines.
- To assess their role in regulating immune cell trafficking in PTB.
Main Methods:
- Cytometric Bead Array (CBA) and ELISA for cytokine/chemokine quantification.
- Flow cytometry for chemokine receptor expression analysis.
- Study included 34 PTB patients and 30 healthy controls.
Main Results:
- Increased levels of IP-10, MIG, IL-8, RANTES, and IL-6 observed in PTB.
- Decreased levels of Interferon-gamma, TNF-alpha, and TGF-beta in PTB.
- Differential expression of chemokine receptors (CCR1, CCR2, CXCR2, CCR7, CXCR3) on immune cells in PTB patients.
Conclusions:
- Chemokines function coordinately and consistently during PTB.
- Peripheral chemokine-cytokine balance influences effector immune cell trafficking.
- Differential chemokine receptor expression may modulate monocyte migration in PTB.
Abstract:
The systemic changes in immune mediators such as cytokine and chemokines, and their synchronized interaction that regulates the cell trafficking during Mycobacterium tuberculosis (M. tuberculosis) infection, were studied. Cytokines and chemokines were evaluated by cytometric bead array (CBA) and enzyme-linked immunosorbent assay (ELISA) in 34 pulmonary tuberculosis (PTB) patients and 30 healthy subjects. The expression of chemokine receptors was assessed by flow cytometry. A significant increase in IP-10, MIG, interleukin-8, RANTES, and interleukin-6 levels was found, whereas a decrease in interferon-gamma, tumor necrosis factor-alpha, and transforming growth factor-beta was observed during PTB. Significant correlation within chemokines and between cytokines was observed in PTB. All immune cells except monocytes and B cells expressed significantly higher levels of CCR1, CCR2, and CXCR2 whereas CCR7 expression was upregulated only on monocytes and neutrophils in PTB. Both T and B cells expressed significantly high levels of CXCR3 which also correlated well with the chemokine levels in PTB. Thus, it was found that chemokines function coordinately and consistently during PTB. This balanced chemokine and cytokine relationship at the periphery may aid in amplified effector immune cell trafficking and retarded monocyte migration through differential chemokine receptor expression.
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