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p-Index From 2021 - 2026
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All Journal Indonesian Journal of Global Health research Synthesis Global Health Journal Indonesian Journal of Global Health Research
Welly Salutondok
Universitas Kristen Indonesia
Education Health Professions Languange, Linguistic, Communication & Media Nursing Public Health

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The Role of Toll-Like Receptor-2 in the Pathogenesis of Pulmonary Tuberculosis Sudarto Sudarto; Zen Hafy; Irsan Saleh; Iche Andriyani Liberty; Zen Ahmad; Fadhyl Zuhry Lubis; Owen Hu; Welly Salutondok
Indonesian Journal of Global Health Research Vol 7 No 3 (2025): Indonesian Journal of Global Health Research
Publisher : GLOBAL HEALTH SCIENCE GROUP

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37287/ijghr.v7i3.6797

Abstract

Pulmonary tuberculosis (PTB), primarily caused by Mycobacterium tuberculosis (M.tb), remains a major global health burden. Toll-like receptor 2 (TLR-2), a critical component of the innate immune system, plays a key role in the host-pathogen interaction by recognizing specific components of the mycobacterial cell wall and initiating downstream inflammatory pathways. However, the dual role of TLR-2 in both protective immunity and immune evasion by M.tb contributes to the complexity of TB pathogenesis. This study aims to investigate the role of Toll-Like Receptor-2 (TLR-2) in the pathogenesis of pulmonary tuberculosis, including its immunological mechanisms, relationships with disease severity, and the potential of TLR-2 as a diagnostic and therapeutic target. This literature review systematically analyzed molecular mechanisms involving TLR-2 signaling in pulmonary TB using peer-reviewed primary and secondary sources from experimental and clinical studies. Emphasis was placed on signal transduction (NF-κB and MAPK), cytokine profiles, antigen presentation, and the impact of TLR-2 gene polymorphisms on TB susceptibility. Activation of TLR-2 through ligands such as lipoproteins, lipoarabinomannan (LAM), and PE/PPE proteins initiates immune responses via MyD88-dependent pathways, leading to the release of proinflammatory cytokines (TNF-α, IL-6, IL-12). TLR-2 also enhances the function of macrophages and dendritic cells, promoting Th1-mediated immunity. However, chronic or excessive stimulation of TLR-2 can suppress antigen processing, promote IL-10 expression, inhibit phagolysosome fusion, and facilitate M. tb survival within host macrophages. Polymorphisms in the TLR-2 gene (e.g., rs3804099) have been associated with increased susceptibility and variable clinical outcomes in PTB. TLR-2 plays a paradoxical role in pulmonary tuberculosis by mediating both protective immunity and facilitating immune evasion by M.tb. Understanding the balance of TLR-2 signaling and genetic variation is crucial for developing immunomodulatory therapies and personalized interventions in TB management.
Navigating Tuberculosis Treatment Challenges of Genetic Perspectives and DNA-Based Detection: A Literature Review Rouly Pola Pasaribu; Zen Hafy; Ariesti Karmila; Nur Riviati; Zen Ahmad; Fadhyl Zuhry Lubis; Welly Salutondok
Indonesian Journal of Global Health Research Vol. 8 No. 4 (2026): Indonesian Journal of Global Health Research
Publisher : GLOBAL HEALTH SCIENCE GROUP

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37287/ijghr.v8i4.1926

Abstract

Tuberculosis remains a major global health problem, particularly because of the increasing burden of drug-resistant tuberculosis (DR-TB), including MDR-TB and XDR-TB. Resistance in Mycobacterium tuberculosis is driven mainly by spontaneous genetic mutations, adaptive evolution, tolerance mechanisms, and host microenvironmental factors, which complicate both treatment and diagnosis. This review aimed to examine recent advances in the genetic mechanisms underlying antibiotic resistance in M. tuberculosis and to evaluate the progress of DNA-based detection technologies for tuberculosis diagnosis and management. This literature review analyzed 49 scientific articles published between 2012 and 2026 to examine the molecular and genetic basis of drug resistance in M. tuberculosis. The study focused on identifying target gene mutations, efflux pump mechanisms, compensatory evolution, and heteroresistance. Furthermore, it evaluated the clinical application of advanced DNA-based diagnostic tools, including GeneXpert, line probe assays, targeted next-generation sequencing (tNGS), whole-genome sequencing (WGS), droplet digital PCR, and CRISPR-based detection. Information was qualitatively synthesized to compare the efficacy and limitations of these modern diagnostic strategies in global tuberculosis management. Drug resistance was primarily associated with de novo mutations in genes such as rpoB, katG, inhA, pncA, gyrA/gyrB, and rrs/eis, as well as compensatory mutations that preserve bacterial fitness. In addition, non-genetic tolerance, dormancy, and efflux pump overexpression contributed to bacterial survival. DNA-based technologies enabled faster and more comprehensive resistance detection than conventional methods, although limitations remained in sensitivity, mutation coverage, cost, and infrastructure requirements. Genetic mutations, evolutionary adaptation, and tolerance mechanisms form the core basis of drug resistance in M. tuberculosis. Integrating DNA-based diagnostics into clinical practice is essential to improve early resistance detection, support personalised treatment, and reduce the spread of drug-resistant tuberculosis.
COMPARATIVE ANALYSIS OF THE EFFECTIVENESS OF OLD AND NEW TB DRUGS IN THE TREATMENT OF PULMONARY TUBERCULOSIS Romauli Lumbantobing; Linggom Kurniaty; Welly Salutondok; Tiroy Sari B. Simanjuntak
SYNTHESIS Global Health Journal Volume 3, Issue 2, 2025
Publisher : SYNTIFIC

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.61543/syn.v3i2.148

Abstract

Background. The availability of effective drug regimens of Pulmonary tuberculosis (TB) poses a global health challenge. Traditional first-line therapies-isoniazid, rifampicin, pyrazinamide, and ethambutol-remain the cornerstone of TB management due to their accessibility and documented cure rates exceeding 85%. Nevertheless, limitations such as variable drug metabolism, patient non-adherence, and the emergence of multidrug-resistant strains have prompted evaluation of newer treatment combinations to optimize efficacy, safety, and duration. The purpose was to compare the effectiveness of older first-line tuberculosis (TB) drug regimens with newer therapeutic regimens in the treatment of pulmonary tuberculosis. Research Method. This narrative review synthesizes findings from five peer-reviewed studies comparing the effectiveness and safety profiles of conventional and novel TB drug regimens. The review focused on regimen composition, treatment duration, bacteriological clearance, hepatotoxicity, and patient adherence outcomes. Findings. The inclusion of pyrazinamide in six-month regimens significantly accelerated bacterial clearance without increasing hepatic toxicity compared to traditional nine-month isoniazid–rifampicin regimens. Additionally, shorter rifampin-based regimens for latent TB demonstrated higher treatment completion rates and fewer adverse effects than isoniazid monotherapy. Emerging regimens, such as fluoroquinolone-based HRM therapies and the novel BPaL combination (bedaquiline, pretomanid, and linezolid), yielded comparable or improved outcomes, with BPaL achieving success rates up to 93% in drug-resistant TB cases. Conclusion. Current evidence supports the strategic adaptation of TB therapy to balance efficacy, tolerability, and treatment duration. Incorporating newer drug combinations, particularly for drug-resistant TB, enhances adherence and clinical outcomes, underscoring the need for individualized treatment protocols aligned with evolving resistance patterns and patient profiles.
Co-Authors Ariesti Karmila Fadhyl Zuhry Lubis Iche Andriyani Liberty, Iche Andriyani Linggom Kurniaty Muhammad Irsan Saleh Nur Riviati Owen Hu Romauli Lumbantobing Rouly Pola Pasaribu Sudarto Sudarto Tiroy Sari B. Simanjuntak Zen Ahmad Zen Ahmad Zen Hafy