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Generation of Lymphocytic Microparticles and Detection of their Proapoptotic Effect on Airway Epithelial Cells
Published on: February 20, 2015
LPO and apoptosis during pulmonary tuberculosis
V V Novitskii1, A K Strelis, S B Tkachenko
1Department of Pathophysiology, Central Research Laboratory, Siberian State Medical University, Russian Federal Agency for Public Health and Social Development, Tomsk.
Bulletin of Experimental Biology and Medicine
|June 9, 2006
Summary
Pulmonary tuberculosis activates lipid peroxidation (LPO) and apoptosis in blood cells. While LPO normalizes post-treatment, apoptosis remains elevated, indicating persistent cellular stress in tuberculosis patients.
Area of Science:
- Biochemistry
- Immunology
- Cell Biology
Background:
- Pulmonary tuberculosis (TB) is an infectious disease affecting the lungs.
- Cellular damage and immune responses are critical in TB pathogenesis.
- Lipid peroxidation (LPO) and apoptosis are key indicators of cellular stress and death.
Purpose of the Study:
- To investigate the role of LPO and apoptosis in mononuclear cells of pulmonary TB patients.
- To assess the impact of standard chemotherapy on LPO and apoptosis during TB treatment.
Main Methods:
- Studied LPO and apoptosis in blood mononuclear cells (lymphocytes and monocytes).
- Analyzed these markers in patients before and during anti-TB chemotherapy.
- Compared marker levels pre-treatment, during treatment, and post-treatment.
Main Results:
- Pulmonary TB was associated with increased LPO and apoptosis in lymphocytes and monocytes.
- These cellular changes were evident both before and after intensive care.
- Post-therapy, LPO levels returned to normal, but apoptosis activity remained significantly high.
Conclusions:
- Standard chemotherapy effectively reduces LPO in TB patients.
- Persistent high apoptosis activity post-treatment suggests ongoing cellular damage or immune dysregulation.
- Further research is needed to understand the implications of sustained apoptosis in TB recovery.
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