Polymorphysm of tumor necrosis factor-Α interleukin-10 gene with pulmonary tuberculosis susceptibility

Main Article Content

Debie Anggraini
Ellyza Nasrul
Rika Susanti
Netti Suharti

Keywords

tumor necrosis factor-A gene; interleukin-10 gene; polymorphism; pulmonary tuberculosis.

Abstract

Pulmonary tuberculosis (TB) is an infectious disease caused by the acid-fast bacterium Mycobacterium tuberculosis (MTB). It is a progressive granulomatous infection, spreading through droplets in the air, and can be fatal. This makes a patient with pulmonary TB a primary source of transmission in the surrounding population. This case-control research was carried out at the Central Laboratory of the Lung Hospital of West Sumatra. The analysis of polymorphisms of the tumor necrosis factor-α (TNF-α) and the interleukin (IL)-10 genes was carried out at the Biomedical Laboratory of the Faculty of Medicine, Andalas University, in collaboration with 1st Base Malaysia. The results indicate that the clinical symptoms of TB can be grouped into either general or specific based on the organ involved. The clinical picture is not always typical, making clinical diagnosis difficult. TNF-α is a cytokine secreted by Th1 cells, macrophages, monocytes, neutrophils, effector T lymphocytes (T cells), and natural killer (NK) cells. It prevents pulmonary TB infection and maintains latent TB status by activating macrophages, transporting them to the site of infection, and forming granulomas that control TB infection. It also prevents the reactivation of persistent TB infection, modulates pulmonary expression of specific immunological factors, and limits the pathological response of the host. During aerosol transmission of MTB, the first cells exposed to the pathogen are alveolar macrophages and pulmonary dendritic cells, which get activated and phagocytose MTB, producing TNF-α and IL-12 cytokines, that in turn activate host antimicrobial mechanisms, and induce IL-10 to inhibit the mechanism.

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