Abstract

Tuberculosis (TB) is one of the highest infectious burdens worldwide, and pathogenesis is yet incompletely elucidated. Bacilli dissemination is due to poor antioxidant defense mechanisms and intensified oxidative stress. There are few recent studies that analyzed and compared free radicals or antioxidant status before and after anti-TB treatment. Hence, the present study underlines the need to identify oxidative stress as it could be a useful tool in TB monitorisation. Thirty newly diagnosed patients with pulmonary TB were included after signing an informed consent. Blood was collected before receiving first-line anti-tubercular therapy (T0) and after 60 days (T2). Spectrophotometric methods were used to quantify oxidative parameters (TBARS—thiobarbituric acid reactive species); enzymatic antioxidants such as SOD (superoxide dismutase), CAT (catalase), GPx (glutathione peroxidase), and TAC (total antioxidant capacity); and non-enzymatic antioxidants such as GSH (reduced glutathione). A moderate positive correlation was found between GSH and TAC (r = 0.63, p-value = 0.046) and GSH and SOD (r = 0.64, p-value = 0.041) at T2. Increased values of GSH, CAT, and SOD were noted at T2 in comparison with T0, while GPx, TAC, and TBARS decreased at T2. A better monitorisation in TB could be based on oxidative stress and antioxidant status. Nevertheless, restoring redox host balance could reduce TB progression.

Highlights

  • The World Health Organisation (WHO) announced in 2019 that, in Europe, 30 people are diagnosed with active tuberculosis (TB) every hour [1]

  • We found that only Vidhya et al analysed oxidative biomarkers status in pulmonary TB patients before and after pharmacotherapy, in the last 5 years, and they suggested that antioxidant co-supplementation could be useful in reducing TB severity [10]

  • The present pilot study underlines the involvement of increased oxidative species and reduction of antioxidant status in developing pulmonary active TB

Read more

Summary

Introduction

The World Health Organisation (WHO) announced in 2019 that, in Europe, 30 people are diagnosed with active tuberculosis (TB) every hour [1]. Identification of oxidative stress involvement in TB could lead to better disease monitorisation [6]. Mycobacterium tuberculosis (M.tb), the aetiological agent of TB, is capable of high and long-term persistence within macrophages by inhibiting phago-lysosomal fusion [3,4,5]. Latent infection appears as a response of M.tb. If alveolar macrophages further attract more immune cells such as monocytes and neutrophils, an inflammatory granuloma will be formed, as M.tb. Within the granuloma, immune cells interact and trigger immune responses in order to control TB, macrophages can undergo respiratory burst, generating oxidative stress and initiating active pulmonary TB [4,7,8]. Bacilli release and infection progression are consequences of lipid peroxidation, parenchymal tissue destruction, and insufficient antioxidant defence mechanisms [3,9,10]. The higher the bacterial load, the more advanced will be the necrosis; an immunological fight between M.tb. and the individual will establish disease consequences [3,9,11,12]

Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call