The role of Mycobacterium tuberculosis complex species on apoptosis and necroptosis state of macrophages derived from ac
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BMC Research Notes Open Access
RESEARCH NOTE
The role of Mycobacterium tuberculosis complex species on apoptosis and necroptosis state of macrophages derived from active pulmonary tuberculosis patients Budi Yanti1,2* , Mulyadi Mulyadi3, Muhammad Amin4, Harapan Harapan5,6, Ni Made Mertaniasih7,8 and Soetjipto Soetjipto8,9*
Abstract Objective: The role of Mycobacterium tuberculosis complex (MTBC) species in tuberculosis (TB) infection in human is still questioned. The aim of this study was to determine whether M. tuberculosis and M. bovis is associated with apoptosis and necroptosis by measuring the expression of specific signaling pathways components (Fas-associated protein with death domain (FADD) and receptor interacting protein 3 (RIP3)), and the level of apoptosis. Results: We recruited 30 patients with pulmonary TB; 24 patients were infected with M. tuberculosis Beijing strain and six patients with M. bovis BCG strain. M. tuberculosis-infected patients were more likely to have severe lung damage compared to those infected with M. bovis (odds ratio [OR] 7.60; 95% confidence interval [CI] 1.07–54.09). M. tuberculosis infection was associated with lower expression of FADD and lower apoptosis level of macrophages compared to M. bovis. No significant different of RIP3 between MTBC species groups. In conclusion, M. tuberculosis Beijing strain was associated with severe pulmonary damage, inhibited FADD expression and reduced apoptosis level of macrophages derived from pulmonary TB patients. This suggests that the M. tuberculosis Beijing strain is potentially to be used as determinant of disease progressivity and tissue damage in TB cases. Keywords: Mycobacterium tuberculosis, Mycobacterium bovis, Apoptosis, Necroptosis, FADD, RIP3 Introduction Mycobacterium tuberculosis complex (MTBC) continues to significantly impact public health and is associated with one million deaths of tuberculosis (TB) cases annually worldwide [1]. Ability of M. tuberculosis to establish disease is entirely depend on macrophage deaths during *Correspondence: [email protected]; [email protected]. ac.id 1 Postgraduate Program, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia 9 Department of Medical Biochemistry, Faculty of Medicine, Universitas Airlangga, Kampus C Mulyorejo Kec. Mulyorejo–Kota, Surabaya, Prov. Jawa Timur 60115, Indonesia Full list of author information is available at the end of the article
infection. Pulmonary macrophages are critical component of the primary innate immune response that have various functions in immune surveillances, removal of cellular debris, microbial clearance, and in resolution of inflammation [2]. There are two pathways of macrophage deaths, apoptosis and necroptosis, that are developed as host antimicrobial defenses in the early TB infection; both of them are programmed cell death [3]. These mechanisms are triggered by tumor necrosis factor alpha (TNFα), oxidative stress, lipopolysaccharide (LPS), and other factors [4]. Apoptosis is characterized by signaling cell th
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