Considerable measures have been implemented in healthcare institutions to screen for and treat tuberculosis (TB) in developed countries; however, in low- and middle-income countries, many individuals still suffer from TB’s deleterious effects. TB is caused by an infection from the Mycobacterium tuberculosis (M. tb) bacteria. Symptoms of TB may range from an asymptomatic latent-phase affecting the pulmonary tract to a devastating active and disseminated stage that can cause central nervous system demise, musculoskeletal impairments, and genitourinary compromise. Following M. tb infection, cytokines such as interferons (IFNs) are released as part of the host immune response. Three main classes of IFNs prevalent during the immune defense include: type I IFN (α and β), type II IFN (IFN-γ), and type III IFN (IFN-λ). The current literature reports that type I IFN plays a role in diminishing the host defense against M. tb by attenuating T-cell activation. In opposition, T-cell activation drives type II IFN release, which is the primary cytokine mediating protection from M. tb by stimulating macrophages and their oxidative defense mechanisms. Type III IFN has a subsidiary part in improving the Th1 response for host cell protection against M. tb. Based on the current evidence available, our group aims to summarize the role that each IFN serves in TB within this literature review.

Mycobacterium avium complex (MAC) infections present significant therapeutic challenges due to their inherent antibiotic resistance, demanding innovative treatment approaches. This study investigated the antimicrobial and antioxidant potential of a novel compound, Fullerene Gallium Phosphonate (FGP), and compared its effects against a previously tested similar compound, Fullerene Disodium Phosphonate (FDSP). Results of experiments using MAC cultures and infected THP-1 macrophages treated with varying FGP and FDSP concentrations (1, 10, 100 µg/mL) revealed that FGP demonstrated greater efficacy than FDSP in reducing M. avium colony-forming units (CFU), achieving a nearly 3-fold reduction by day 8, compared to a 2-fold decrease with FDSP. In infected macrophages, FGP significantly decreased bacterial load at 1 and 10 µg/mL (p < 0.01). FGP also lowered oxidative stress, reflected by a significant reduction in malondialdehyde (MDA) levels on day 4 (p < 0.05) and decreased IL-6 (2-fold) and TNF-α levels (3-fold) by day 8, indicating both antimicrobial and anti-inflammatory effects. However, FGP paradoxically increased MAC burden at its highest concentration and showed no significant difference in efficacy of different concentrations. These findings suggest that FGP may serve as a promising candidate for antimycobacterial therapy with dual antibacterial and antioxidant effects. Further research is crucial to fully elucidate its mechanism of action and find the optimal therapeutic window.