Suppression of Mycobacterium Tuberculosis Induced Reactive Oxygen Species andTumor Necrosis Factor-Alpha Activity in Human Monocytes of Systemic LupusErythematosus Patients by Reduced Glutathione

 Objectives: The etiology and pathogenesis of systemic lupuserythematosus remains unknown, evidence exists for theinvolvement of mycobacterial antigen. This study is aimed todetermine the effect of Mycobacterium tuberculosis on clinicalcourse of SLE patients and the role of ROS and TNF-α in thepatho...

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Bibliographic Details
Main Authors: Najmul Islam, Shah Farhan Azfar
Format: Article
Language:English
Published: Oman Medical Specialty Board 2012-01-01
Series:Oman Medical Journal
Subjects:
Online Access:http://journals.indexcopernicus.com/fulltxt.php?ICID=982315
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Summary: Objectives: The etiology and pathogenesis of systemic lupuserythematosus remains unknown, evidence exists for theinvolvement of mycobacterial antigen. This study is aimed todetermine the effect of Mycobacterium tuberculosis on clinicalcourse of SLE patients and the role of ROS and TNF-α in thepathogenesis of tuberculosis associated SLE patients.Methods: This study was done on 100 patients divided intoSLE group (n=30), TB group (n=30), SLE-TB group (n=30) andcontrol group (n=10). All patients underwent clinical, biochemicaland immunological evaluation by employing techniques such asSDS-PAGE, direct binding and competition ELISA, PBMC andcell culture.Results: Fever, arthritis, skin rash, photosensitivity were morecommon in both SLE and SLE-TB group. Reduced glutathioneshowed amelioration of ROS and TNF-α induced action, which inturn, subsequently suppressed the immune-bindings observed inmonocytes of TB and SLE patients cultured without glutathione.Conclusion: Data shows that SLE patients are more susceptible todeveloping Mycobacterium tuberculosis, as ROS and TNF-α in SLEpatients could activate the replication of mycobacterial Ag85B (30kDa) after bacilli infection.
ISSN:1999-768X
2070-5204