T, Wibawa, Lisa, Pangemanan, FJ, Rachmawaty, N, Rintiswati, Mustofa, - and MH, Soesatyo (2014) Isoniazid (INH) treatment of INH-resistant Mycobacterium tuberculosis inhibits infected macrophage to produce TNF-alpha. Isoniazid (INH) treatment of INH-resistant Mycobacterium tuberculosis inhibits infected macrophage to produce TNF-alpha, 45 (5). pp. 1107-1113. ISSN 2541-7512, Jurnal Internasional bereputasi Q3, SJR (2014): 0,394
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Abstract
Macrophages undergo apoptosis after infected by Mycobacterium tuberculosis (M.tb), which is regulated by tumor necrosis factor α (TNF-α) and has a direct correlation with killing of intracellular bacilli. In order to clarify the role of isoniazid (INH) in the modulation of macrophages apoptosis and intracellular bacilli replication, we performed the following studies using an INH-resistant clinical M.tb isolate (INHres). Macrophages derived from peripheral blood were infected with INHres and treated or not treated with INH. Apoptosis was measured using an Ag-capture ELISA for histone and fragmented DNA. Production of TNF-α by INHres infected was assayed using ELISA and viability of intracellular M.tb was determined using bacterial culture of macrophage lysates on Löwenstein-Jensen (LJ) medium. INH pre-treatment to INHres reduced macrophages apoptosis, production of TNF-α and intracellular INHres viability. This study indicated that INH affected TNF-α release resulting in reduction of the extent macrophages apoptosis and of intracellular INH-resistant M.tb viability.
Item Type: | Article |
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Uncontrolled Keywords: | Mycobacterium tuberculosis, apoptosis, isoniazid, macrophage |
Subjects: | Medicine |
Divisions: | Journal Publication |
Depositing User: | F.X. Hadi |
Date Deposited: | 19 Jan 2021 05:28 |
Last Modified: | 17 Feb 2021 05:41 |
URI: | https://repository.ukwms.ac.id/id/eprint/24087 |
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