The Interplay Between Systemic Inflammation, Oxidative Stress, and Tissue Remodeling in Tuberculosis

被引:55
作者
Amaral, Eduardo P. [1 ]
Vinhaes, Caian L. [2 ,3 ,4 ]
Oliveira-de-Souza, Deivide [2 ,3 ,4 ]
Nogueira, Betania [3 ,4 ,5 ]
Akrami, Kevan M. [3 ,5 ,6 ]
Andrade, Bruno B. [2 ,3 ,4 ,7 ,8 ,9 ,10 ]
机构
[1] NIAID, Immunobiol Sect, Lab Parasit Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA
[2] Fundacao Oswaldo Cruz, Inst Goncalo Moniz, Lab Inflamacao & Biomarcadores, Rua Waldemar Falcao 121, BR-40296710 Salvador, BA, Brazil
[3] Multinatl Org Network Sponsoring Translat & Epide, Salvador, BA, Brazil
[4] Fac Tecnol & Ciencias FTC, Curso Med, Salvador, BA, Brazil
[5] Univ Fed Bahia, Fac Med, Salvador, BA, Brazil
[6] Univ Calif San Diego, Dept Med, Div Infect Dis & Pulm Crit Care & Sleep Med, San Diego, CA 92103 USA
[7] Univ Cape Town, Wellcome Ctr Infect Dis Res Africa, Inst Infect Dis & Mol Med, Cape Town, South Africa
[8] Vanderbilt Univ, Sch Med, Dept Med, Div Infect Dis, Nashville, TN 37212 USA
[9] Univ Salvador UNIFACS, Laureate Univ, Salvador, BA, Brazil
[10] Ecola Bahiana Med & Saude Publ EBMSP, Salvador, BA, Brazil
关键词
tuberculosis; reactive oxygen species; oxidative stress; heme oxygenase; matrix metalloproteinase; tissue remodeling; TUMOR-NECROSIS-FACTOR; ACTIVE PULMONARY TUBERCULOSIS; BLOOD MONONUCLEAR-CELLS; MYCOBACTERIUM-TUBERCULOSIS; LIPID-PEROXIDATION; HEME OXYGENASE-1; VITAMIN-E; MATRIX METALLOPROTEINASE-1; INNATE IMMUNITY; CATHEPSIN K;
D O I
10.1089/ars.2020.8124
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Significance:Excessive and prolonged proinflammatory responses are associated with oxidative stress, which is commonly observed during chronic tuberculosis (TB). Such condition favors tissue destruction and consequently bacterial spread. A tissue remodeling program is also triggered in chronically inflamed sites, facilitating a wide spectrum of clinical manifestations. Recent Advances:Since persistent and exacerbated oxidative stress responses have been associated with severe pathology, a number of studies have suggested that the inhibition of this augmented stress response by improving host antioxidant status may represent a reasonable strategy to ameliorate tissue damage in TB. Critical Issues:This review summarizes the interplay between oxidative stress, systemic inflammation and tissue remodeling, and its consequences in promoting TB disease. We emphasize the most important mechanisms associated with stress responses that contribute to the progression of TB. We also point out important host immune components that may influence the exacerbation of cellular stress and the subsequent tissue injury. Future Directions:Further research should reveal valuable targets for host-directed therapy of TB, preventing development of severe immunopathology and disease progression.
引用
收藏
页码:471 / 485
页数:15
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