Abstract
Tuberculosis (TB) is one of the ten leading causes of death worldwide. Patients with TB have been observed to suffer from depression and anxiety linked to social variables. Previous experiments found that the substantial pulmonary inflammation associated with TB causes neuroinflammation, neuronal death, and behavioral impairments in the absence of brain infection. Curcumin (CUR) is a natural product with antioxidant, anti-inflammatory and antibacterial activities. In this work, we evaluated the CUR effect on the growth control of mycobacteria in the lungs and the anti-inflammatory effect in the brain using a model of progressive pulmonary TB in BALB/c mice infected with drug-sensitive mycobacteria (strain H37Rv). The results have shown that CUR decreased lung bacilli load and pneumonia of infected animals. Finally, CUR significantly decreased neuroinflammation (expression of TNFα, IFNγ and IL12) and slightly increased the levels of nuclear factor erythroid 2-related to factor 2 (Nrf2) and the brain-derived neurotrophic factor (BDNF) levels, improving behavioral status. These results suggest that CUR has a bactericidal effect and can control pulmonary mycobacterial infection and reduce neuroinflammation. It seems that CUR has a promising potential as adjuvant therapy in TB treatment.
Highlights
Tuberculosis (TB), the oldest human pandemic, generally caused by infection via the lung with Mycobacterium tuberculosis (Mtb), remains the foremost cause of death among bacterial infectious diseases [1,2]
Tuberculous animals were given CUR (16 or 32 μg/mL) via an intraperitoneal route starting on day 14 after infection to see how these treatments affected the progression of lung disease in BALB/c mice after endotracheal infection with a high dose of the Mtb H37Rv strain, trying to find a dose that reduced neuroinflammation without aggravating loads in the lungs and brains, the Mtb-infected animals’ survival and pneumonia
By RT-PCR, we investigated the effects of CUR vs. saline solution on TNFα, IFNγ, and IL-12 expression in the hippocampus, hypothalamus, cerebellum, and frontal cortex of mice infected with Mtb
Summary
Tuberculosis (TB), the oldest human pandemic, generally caused by infection via the lung with Mycobacterium tuberculosis (Mtb), remains the foremost cause of death among bacterial infectious diseases [1,2]. Bacillus Calmette–Guérin (BCG), a live attenuated strain of Mycobacterium bovis [3], the primary cause of bovine TB [4], is the only approved vaccine against TB and is the most widely used vaccine in history [4,5]. Though billions of individuals were vaccinated in the past century, TB remains a severe threat to global health [5]. Due to the COVID-19 pandemic, the number of deaths attributable to TB is expected to increase to similar levels presented in 2012, increasing to between 200,000 and 400,000 deaths (1.6–1.8 million deaths) [6]. The COVID-19 pandemic and related lockdown restrictions significantly impacted providing and monitoring TB surveillance strategies globally [7]
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