Polymorphysm of tumor necrosis factor-Α interleukin-10 gene with pulmonary tuberculosis susceptibility (Turnitin Version)

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.