Role of toll-like receptors in tuberculosis infection

Biyikli O. O., Baysak A. G., Ece G., Oz A. T., Ozhan M. H., Berdeli A.

Jundishapur Journal of Microbiology, vol.9, no.10, 2016 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 9 Issue: 10
  • Publication Date: 2016
  • Doi Number: 10.5812/jjm.20224
  • Journal Name: Jundishapur Journal of Microbiology
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Keywords: Genetic polymorphism, Infection, Mycobacterium tuberculosis, Toll-like receptor
  • Istanbul Medipol University Affiliated: No


Background: One-third of the world’s population is infected with Mycobacterium tuberculosis. Investigation of Toll-like receptors (TLRs) has revealed new information regarding the immunopathogenesis of this disease. Toll-like receptors can recognize various ligands with a lipoprotein structure in the bacilli. Toll-like receptor 2 and TLR-4 have been identified in association with tuberculosis infection. Objectives: The aim of our study was to investigate the relationship between TLR polymorphism and infection progress. Methods: Twenty-nine patients with a radiologically, microbiologically, and clinically proven active tuberculosis diagnosis were included in this 25-month study. Toll-like receptor 2 and TLR-4 polymorphisms and allele distributions were compared between these 29 patients and 100 healthy control subjects. Peripheral blood samples were taken from all patients. Genotyping of TLR-2, TLR-4, and macrophage migration inhibitory factor was performed. The extraction step was completed with a Qiagen mini blood purification system kit (Qiagen, Ontario, Canada) using a peripheral blood sample. The genotyping was performed using polymerase chain reaction-restriction fragment length polymorphism. Results: In total, 19 of the 29 patients with tuberculosis infection had a TLR-2 polymorphism, and 20 of the 100 healthy subjects had a TLR-2 polymorphism (P < 0.001). The TLR-4 polymorphism and interferon-γ allele distributions were not statistically correlated. Conclusions: Toll-like receptor 2 polymorphism is a risk factor for tuberculosis infection. The limiting factor in this study was the lack of investigation of the interferon-γ and tumor necrosis factor-α levels, which are important in the development of infection. Detection of lower levels of these cytokines in bronchoalveolar lavage specimens, especially among patients with TLR-2 defects, will provide new data that may support the results of this study.