Role of NF-κB during Mycobacterium tuberculosis Infection

• Published in: International journal of molecular sciences Vol. 24; no. 2; p. 1772
• Main Authors: Poladian, Nicole, Orujyan, Davit, Narinyan, William, Oganyan, Armani K, Navasardyan, Inesa, Velpuri, Prathosh, Chorbajian, Abraham, Venketaraman, Vishwanath
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 16-01-2023; MDPI
• Subjects: Antigens; Cell activation; Cytokines; Dendritic cells; Granuloma; Granulomas; Humans; Hypoxia; Immune system; Infections; Inflammation; Inflammatory diseases; Inflammatory response; Interleukin 1; Interleukin 10; Interleukin 12; Interleukin 2; Interleukin 2 receptors; Interleukin 6; Intracellular signalling; Kinases; Latent infection; Literature reviews; Low income groups; Lymphocytes B; Macrophages; Medical prognosis; Mycobacterium tuberculosis; Mycobacterium tuberculosis - metabolism; NF-kappa B - metabolism; NF-κB; NF-κB protein; Pathogens; Pattern recognition; Phosphorylation; Review; rifampicin; Transcription factors; Tuberculosis; Tuberculosis - microbiology; Tumor Necrosis Factor-alpha - metabolism; Tumor necrosis factor-TNF; Tumor necrosis factor-α; γ-Interferon; United States > US; NF-κB; rifampicin; isoniazid; Mycobacterium tuberculosis; inflammation; ethambutol; granuloma; pyrazinamide; cytokines
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms24021772

(
) causes tuberculosis infection in humans worldwide, especially among immunocompromised populations and areas of the world with insufficient funding for tuberculosis treatment. Specifically,
is predominantly exhibited as a latent infection, which poses a greater risk of reactivation for infected individuals. It has been previously shown that
infection requires pro-inflammatory and anti-inflammatory mediators to manage its associated granuloma formation via tumor necrosis factor-α (TNF-α), interleukin-12 (IL-12), interferon-γ (IFN-γ), and caseum formation via IL-10, respectively. Nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) has been found to play a unique mediator role in providing a pro-inflammatory response to chronic inflammatory disease processes by promoting the activation of macrophages and the release of various cytokines such as IL-1, IL-6, IL-12, and TNF-α. NF-κB's role is especially interesting in its mechanism of assisting the immune system's defense against
, wherein NF-κB induces IL-2 receptors (IL-2R) to decrease the immune response, but has also been shown to crucially assist in keeping a granuloma and bacterial load contained. In order to understand NF-κB's role in reducing
infection, within this literature review we will discuss the dynamic interaction between
and NF-κB, with a focus on the intracellular signaling pathways and the possible side effects of NF-κB inactivation on
infection. Through a thorough review of these interactions, this review aims to highlight the role of NF-κB in
infection for the purpose of better understanding the complex immune response to
infection and to uncover further potential therapeutic methods.