Chinta Krishna C, Pacl Hayden T, Agarwal Anupam, Steyn Adrie J C
Department of Microbiology, School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Division of Nephrology, School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Antioxidants (Basel). 2021 Jan 26;10(2):177. doi: 10.3390/antiox10020177.
Excessive inflammation and tissue damage are pathological hallmarks of chronic pulmonary tuberculosis (TB). Despite decades of research, host regulation of these clinical consequences is poorly understood. A sustained effort has been made to understand the contribution of heme oxygenase-1 (HO-1) to this process. HO-1 is an essential cytoprotective enzyme in the host that controls inflammation and oxidative stress in many pathological conditions. While HO-1 levels are upregulated in animals and patients infected with (), how it regulates host responses and disease pathology during TB remains unclear. This lack of clarity is due in part to contradictory studies arguing that HO-1 induction contributes to both host resistance as well as disease progression. In this review, we discuss these conflicting studies and the role of HO-1 in modulating myeloid cell functions during disease progression. We argue that HO-1 is a promising target for host-directed therapy to improve TB immunopathology.
过度炎症反应和组织损伤是慢性肺结核（TB）的病理特征。尽管经过数十年研究，但对这些临床后果的宿主调控机制仍知之甚少。人们一直在持续努力了解血红素加氧酶-1（HO-1）在这一过程中的作用。HO-1是宿主体内一种重要的细胞保护酶，在许多病理状况下可控制炎症和氧化应激。虽然在感染（）的动物和患者中HO-1水平会上调，但在结核病期间它如何调节宿主反应和疾病病理仍不清楚。这种不明确部分是由于相互矛盾的研究，这些研究认为HO-1的诱导既有助于宿主抵抗，也会促进疾病进展。在本综述中，我们讨论了这些相互矛盾的研究以及HO-1在结核病疾病进展过程中调节髓样细胞功能的作用。我们认为HO-1是改善结核病免疫病理学的宿主导向治疗的一个有前景的靶点。
