Melola Discovery

← Melola Discovery

Open access Journal SINTA 1

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

Indonesian Journal of Biotechnology · Vol. 11 No. 1 (2006) · pp. 895–900

DOI
10.22146/ijbiotech.16387
ISSN
2089-2241, 0853-8654
Published
2006-06-01
Publisher
Universitas Gadjah Mada
Language
eng
License
creativecommons.org/licenses/by-sa/4.0

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

Collaboration network of the authors

37 authors · 111 co-authorship links · 4 across different organisations

Hover or tap a name to highlight its co-authors. Double-click to open the author's page.

  • Universitas Gadjah Mada
  • Universitas Muhammadiyah Semarang
  • Tadulako University
  • Kementerian Kesehatan Republik Indonesia
  • Affiliation unknown
  • Different organisations
  • Same organisation
  • Affiliation unknown
  • Thicker line = more joint articles · bigger circle = more articles
Show as table
Co-authorOrganisationJoint articles
Nastiti WijayantiAffiliation unknown3
Jaka WidadaUniversitas Gadjah Mada2
Hera NirwatiAffiliation unknown2
Diani MentariAffiliation unknown1
Nastiti WijayantiUniversitas Gadjah Mada1
Apon Zaenal MustopaAffiliation unknown1
Huda Salahudin DarusmanAffiliation unknown1
Muh. Chaeril IkramullahAffiliation unknown1
Ai HertatiAffiliation unknown1
Rifqiyah Nur UmamiAffiliation unknown1
Lita Tri RatnaAffiliation unknown1
Shasmita IrawanAffiliation unknown1
Moh Egy Rahman FirdausAffiliation unknown1
Aris HaryantoAffiliation unknown1
S. SutaryoAffiliation unknown1
Abdul Rahman SiregarAffiliation unknown1
Abu Tholib AmanAffiliation unknown1
Yati SoenartoAffiliation unknown1
Erni MartaniAffiliation unknown1
Arifah KhusnuryaniAffiliation unknown1
Widya AsmaraUniversitas Gadjah Mada1
Ning RintiswatiAffiliation unknown1
Hardyanto SoebonoAffiliation unknown1
Mustofa MustofaTadulako University1
Maya Dian RakhmawatieUniversitas Muhammadiyah Semarang1
Puspita LisdiyantiAffiliation unknown1
Kanti RatnaningrumAffiliation unknown1
Muhammad Mucharom Chairul UmamAffiliation unknown1
Muhammad Hasan AlfiAffiliation unknown1
Listya ChaririAffiliation unknown1
Mohamad Saifudin HakimAffiliation unknown1
Anika PrastyowatiAffiliation unknown1
Mirna WidiyantiAffiliation unknown1
Holy Arif WibowoKementerian Kesehatan Republik Indonesia1

Affiliations come from OpenAlex; journal OAI-PMH metadata carries none. Authors without an OpenAlex ID are matched by name, which can merge or split people.

Metadata source: OAI-PMH (metadata jurnal) https://jurnal.ugm.ac.id/ijbiotech/oai, first harvested 8 Nov 2026, last seen 8 Nov 2026.
Original metadata (oai_dc) 
<oai_dc:dc xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/  http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
	<dc:title xml:lang="en-US">Apoptosis and Phagocytosis Activity of Macrophages Infected by Mycobacterium tuberculosis Resistant and Sensitive Isoniazid Clinical Isolates</dc:title>
	<dc:creator>Rachmawaty, Farida J.</dc:creator>
	<dc:creator>Wibawa, Tri</dc:creator>
	<dc:creator>Soesatyo, Marsetyawan H. N. E.</dc:creator>
	<dc:subject xml:lang="en-US">Mycobacterium tuberculosis; apoptosis; phagocytosis; macrophages; isoniazid</dc:subject>
	<dc:description xml:lang="en-US">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.</dc:description>
	<dc:publisher xml:lang="en-US">Universitas Gadjah Mada</dc:publisher>
	<dc:contributor xml:lang="en-US"></dc:contributor>
	<dc:date>2006-06-01</dc:date>
	<dc:type>info:eu-repo/semantics/article</dc:type>
	<dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
	<dc:type xml:lang="en-US">Original Research Articles</dc:type>
	<dc:format>application/pdf</dc:format>
	<dc:identifier>https://journal.ugm.ac.id/ijbiotech/article/view/16387</dc:identifier>
	<dc:identifier>10.22146/ijbiotech.16387</dc:identifier>
	<dc:source xml:lang="en-US">Indonesian Journal of Biotechnology; Vol 11, No 1 (2006); 895-900</dc:source>
	<dc:source>2089-2241</dc:source>
	<dc:source>0853-8654</dc:source>
	<dc:language>eng</dc:language>
	<dc:relation>https://journal.ugm.ac.id/ijbiotech/article/view/16387/10903</dc:relation>
	<dc:rights xml:lang="en-US">Copyright (c) 2016 Farida J. Rachmawaty, Tri Wibawa, Marsetyawan H. N. E. Soesatyo</dc:rights>
	<dc:rights xml:lang="en-US">http://creativecommons.org/licenses/by-sa/4.0</dc:rights>
</oai_dc:dc>