Melola Discovery

← Melola Discovery

Akses terbuka Jurnal 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) · hlm. 895–900

DOI
10.22146/ijbiotech.16387
ISSN
2089-2241, 0853-8654
Terbit
2006-06-01
Penerbit
Universitas Gadjah Mada
Bahasa
eng
Lisensi
creativecommons.org/licenses/by-sa/4.0

Abstrak

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.

Kata kunci

Jaringan kolaborasi para penulis

37 penulis · 111 tautan kepenulisan bersama · 4 lintas organisasi

Arahkan kursor atau ketuk sebuah nama untuk menyorot rekan penulisnya. Klik dua kali untuk membuka halaman penulis.

  • Universitas Gadjah Mada
  • Universitas Muhammadiyah Semarang
  • Tadulako University
  • Kementerian Kesehatan Republik Indonesia
  • Afiliasi tidak diketahui
  • Organisasi berbeda
  • Organisasi sama
  • Afiliasi tidak diketahui
  • Garis lebih tebal = lebih banyak artikel bersama · lingkaran lebih besar = lebih banyak artikel
Tampilkan sebagai tabel
Rekan penulisOrganisasiArtikel bersama
Nastiti WijayantiAfiliasi tidak diketahui3
Jaka WidadaUniversitas Gadjah Mada2
Hera NirwatiAfiliasi tidak diketahui2
Diani MentariAfiliasi tidak diketahui1
Nastiti WijayantiUniversitas Gadjah Mada1
Apon Zaenal MustopaAfiliasi tidak diketahui1
Huda Salahudin DarusmanAfiliasi tidak diketahui1
Muh. Chaeril IkramullahAfiliasi tidak diketahui1
Ai HertatiAfiliasi tidak diketahui1
Rifqiyah Nur UmamiAfiliasi tidak diketahui1
Lita Tri RatnaAfiliasi tidak diketahui1
Shasmita IrawanAfiliasi tidak diketahui1
Moh Egy Rahman FirdausAfiliasi tidak diketahui1
Aris HaryantoAfiliasi tidak diketahui1
S. SutaryoAfiliasi tidak diketahui1
Abdul Rahman SiregarAfiliasi tidak diketahui1
Abu Tholib AmanAfiliasi tidak diketahui1
Yati SoenartoAfiliasi tidak diketahui1
Erni MartaniAfiliasi tidak diketahui1
Arifah KhusnuryaniAfiliasi tidak diketahui1
Widya AsmaraUniversitas Gadjah Mada1
Ning RintiswatiAfiliasi tidak diketahui1
Hardyanto SoebonoAfiliasi tidak diketahui1
Mustofa MustofaTadulako University1
Maya Dian RakhmawatieUniversitas Muhammadiyah Semarang1
Puspita LisdiyantiAfiliasi tidak diketahui1
Kanti RatnaningrumAfiliasi tidak diketahui1
Muhammad Mucharom Chairul UmamAfiliasi tidak diketahui1
Muhammad Hasan AlfiAfiliasi tidak diketahui1
Listya ChaririAfiliasi tidak diketahui1
Mohamad Saifudin HakimAfiliasi tidak diketahui1
Anika PrastyowatiAfiliasi tidak diketahui1
Mirna WidiyantiAfiliasi tidak diketahui1
Holy Arif WibowoKementerian Kesehatan Republik Indonesia1

Afiliasi berasal dari OpenAlex; metadata OAI-PMH jurnal tidak memuatnya. Penulis tanpa ID OpenAlex dicocokkan berdasarkan nama, sehingga dua orang bisa tergabung atau satu orang bisa terpisah.

Sumber metadata: OAI-PMH (metadata jurnal) https://jurnal.ugm.ac.id/ijbiotech/oai, pertama di-harvest 8 Nov 2026, terakhir terlihat 8 Nov 2026.
Metadata asli (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>