Apoptosis and Phagocytosis Activity of Macrophages Infected by Mycobacterium tuberculosis Resistant and Sensitive Isoniazid Clinical Isolates

https://doi.org/10.22146/ijbiotech.16387

Farida J. Rachmawaty(1), Tri Wibawa(2*), Marsetyawan H. N. E. Soesatyo(3)

(1) Graduate School of Tropical Medicine, Gadjah Mada University School of Medicine, Yogyakarta 55281, Indonesia.
(2) Department of Microbiology, Gadjah Mada University School of Medicine, Yogyakarta 55281, Indonesia.
(3) Department of Histology and Cell Biology, Gadjah Mada University School of Medicine, Yogyakarta 55281, Indonesia.
(*) Corresponding Author

Abstract


Mycobacterium tuberculosis (M.tb) is the main causative pathogen that cause the pulmonary tuberculosis.
Intracellular M.tb was reported able to induce macrophages apoptosis, which may have crucial role in the regulation
of immun response against M.tb infection. As an intracellular bacteria, M.tb able to live and replicate within
macrophages. Phagocytosis is the first step to achieved this condition. The induction of macrophages apoptosis by
INH resistant and sensitive M.tb clinical isolates, and H37Rv was studied. The macrophages apoptosis level were
measured using an Ag-capture ELISA for histone and fragmented DNA (Cell Death Detection ELISAplus, Roche
Diagnostic GmBH). Phagocytosis activity also analyzed, after staining using fluorescence dye (AcriFluorTM, Scientific
Device Lab.). The results showed that there was no significantly different between INH resistant and sensitive M.tb
clinical isolates in respect their ability to induce apoptosis. The phagocytosis activity among the clinical isolates was
shown to be strain dependent, and undistinguishable between the Mtb clinical isolates. There was no association
between macrophages apoptosis level and the phagocytosis activity. These data suggested that among the virulent
Mtb clinical isolates, the ability to induce macrophages apoptosis and phagocytosis were consistently in comparable
level

Keywords


Mycobacterium tuberculosis; apoptosis; phagocytosis; macrophages; isoniazid

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DOI: https://doi.org/10.22146/ijbiotech.16387

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