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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References

Freixo, I.M., Caldas, P.C.S., Martins, F., Brito, R.C., Ferreira, R.M.C., Fonseca, L.S. and Saad, M.H.F., 2002. Evaluation of Etest strips for rapid susceptibility testing of Mycobacterium tuberculosis. J. Clin. Microbiol., 40, 2282-2284.

Hunter, S.W., and Brennan, P.J., 1990. Evidence for the presence of a phosphatidylinositol anchor on the lipoarabinomannan and lipomannan of Mycobacterium tuberculosis. J. Biol. Chem., 265, 9272–9279.

Kang, P.B., Azad, A.K.,Torrelles, J.B., Kaufman, T.M., Beharka, A., Tibesar, E., DesJardin, L.E., and Schlesinger, L.S., 2005. The human  macrophage  m a n n o s e r e c e p t o r d i r e c t s M y c o b a c t e r i u m  t u b e r c u l o s i s l i p o a r a b i n o m a n n a n - m e d i a t e d phagosome biogenesis. J. Exp. Med., 202, 987–999.

Keane, J., Balcewicz-Sablinska, M.K., Remold, H.G., Chupp, G.L., Meek, B.B., Fenton, M.J., and Kornfeld, H., 1997. Infection by Mycobacterium tuberculosis promotes human alveolar macrophage apoptosis. Infect. Immun., 65, 298–304.

Keane, J., Remold, H.G., and Kornfeld, H., 2000 . Virulent Mycobacterium tuberculosis strains evade apoptosis of infected alveolar macrophages, J. Immunol., 164, 2016-2020.

Klingler, K., Tchou-Wong, K.M., Brandli, O., Aston, C., Kim, R., Chi, C., and Rom, W.N., 1997. Effect of mycobacteria on r e g u l a t i o n o f a p o p t o s i s i n mononuclear phagocytes. Infect. Immun. 65, 5272-5278.

Molloy, A., Laochumroonvorapong, P., and Kaplan, G., 1994. Apoptosis, but not necrosis, of infected monocytes is coupled with killing of intracellular bacillus Calmette-Guerin. J. Exp. Med. 180, 1499–1509.

Oddo, M., Renno, T., Attinger, A., Bakker, T., MacDonald, H.R., and Meylan, P.R.A., 1998. Fas ligand-induced apoptosis of infected human macrophages reduces t h e v i a b i l i t y o f i n t r a c e l l a r

 

WHO. (2005). Global tuberculosis control: surveillance, planning, financing. W H O r e p o r t 2 0 0 5 . G e n e v a , WHO/HTM/TB/2005.349.

Zhang, Y., 2004. Isoniazid, In: Rom WN and Mycobacterium tuberculosis. J. Immunol., Garay   ST   eds.   Tuberculosis   2nd ed., 160, 5448-5454.

Placido, R., Mancino, G., Amendola, A., Mariani, F., Vendetti, S., Piacentini, M., Sanduzzi, A., Bocchino, M. L., Zembala, M., and Colizzi,  V.1997.  A p o p t o s i s    o f    h u m a n         m o n o c y t e s / m a c r o p h a g e s i n Mycobacterium tuberculosis infection. J. Pathol., 181, 31-38.

Schlesinger, L.S., 1993. Macrophages phagocytosis of virulent but not attenuated strain of M. tuberculosis is mediated by mannose receptors in addition to complement receptors. J. Immunol., 2, 659-669.

Slayden, R.A., and Barry, C.E., 2000, The genetics and biochemistry of INH resistance in M. tuberculosis. Microb. Infect., 2, 659-669.

Stokes, R.W., Norris-Jones, R., Brooks, D.E., Beveridge, T.J., Doxsee, D., and Thorson, L.M., 2004. The glycan-rich outer layer of the cell wall of Mycobacterium tuberculosis acts as an antiphagocytic capsule limiting the association of the bacterium with macrophages. Infect. Immun., 72, 5676-5686.

Takayama, K., Wang, L., and David, H.L., 1972. Effect of Isoniazid on the in vivo mycolic acid synthesis, cell growth, viability of Mycobacterium tuberculosis. Antimicrob Agents Chemother., 2, 29-35.

WHO. (2004). Anti-tuberculosis drug resistance in the world: Third global report, The WHO/IUATLD Global Project  on  Anti-tuberculosis  Drug R e s i s t a n c e S u r v e i l l a n c e , WHO/HTM/TB/2004.343.


Lippincott Williams & Wilkins, Philadelpia, pp: 739-758.



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

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