Cytokine Dynamics and Oxidative Stress in Host Cells Stimulated with Drug-Resistant and Sensitive Mycobacterium tuberculosis Isolates
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Background
The immune response to Mycobacterium tuberculosis (M. tuberculosis) is central to the pathogenesis of tuberculosis (TB), yet the immune dynamics induced by drug-resistant strains remain underexplored. Understanding the host’s immune response to both drug-sensitive and drug-resistant M. tuberculosis isolates is crucial for elucidating the mechanisms of pathogenesis and resistance. This study aims to assess the cellular immune responses, including PBMC proliferation, cytokine secretion (IL-4 and IL-17a), and reactive oxygen species (ROS) production in response to live drug-sensitive and drug-resistant M. tuberculosis clinical isolates.
Methods
Peripheral blood mononuclear cells (PBMCs) from PPD-negative and PPD-positive healthy volunteers were stimulated with live M. tuberculosis isolates, including MDR, SI-resistant, and sensitive strains. The immune responses were assessed by evaluating cell proliferation, secretion of IL-4 and IL-17a cytokines, and ROS production over a 9-day period.
Results
PBMCs from PPD-positive individuals exhibited a higher proliferative response compared to PPD-negative individuals, indicating more robust immune memory. IL-4 secretion was low but varied among samples, with higher levels observed in response to MDR isolates, suggesting a potential role in immunopathology. IL-17a levels increased over time, particularly in PPD-positive individuals, and MDR strains elicited a stronger response than sensitive isolates. ROS production was significantly elevated in response to resistant strains, reflecting the host’s oxidative defense mechanisms.
Conclusion
This study demonstrates distinct immune responses to drug-resistant M. tuberculosis isolates, with variations in cell proliferation, cytokine secretion, and ROS production. These findings provide insights into the immune dynamics during infection with resistant strains and underscore the importance of genotype-environment interactions in TB pathogenesis.
