Exploring the Use of Medicinal Plants and Their Bioactive Derivatives as Alveolar NLRP3 Inflammasome Regulators during <i>Mycobacterium tuberculosis</i> Infection

• Main Authors: Nontobeko E. Mvubu, Thamsanqa E. Chiliza
• Format: Article
• Language: English
• Published: MDPI AG 2021-08-01
• Series: International Journal of Molecular Sciences
• Subjects: NLRP3 inflammasomes; alveolar macrophages; pulmonary epithelial cells; medicinal plants; medicinal plant derivatives; <i>Mycobacterium tuberculosis</i>
• Online Access: https://www.mdpi.com/1422-0067/22/17/9497
• ISSN: 1661-6596; 1422-0067

<i>Mycobacterium tuberculosis</i>, the causative agent of tuberculosis (TB), is a successful intracellular pathogen that is responsible for the highest mortality rate among diseases caused by bacterial infections. During early interaction with the host innate cells, <i>M. tuberculosis</i> cell surface antigens interact with Toll like receptor 4 (TLR4) to activate the nucleotide-binding domain, leucine-rich-repeat containing family, pyrin domain-containing 3 (NLRP3) canonical, and non-canonical inflammasome pathways. NLRP3 inflammasome activation in the alveoli has been reported to contribute to the early inflammatory response that is needed for an effective anti-TB response through production of pro-inflammatory cytokines, including those of the Interleukin 1 (IL1) family. However, overstimulation of the alveolar NLRP3 inflammasomes can induce excessive inflammation that is pathological to the host. Several studies have explored the use of medicinal plants and/or their active derivatives to inhibit excessive stimulation of the inflammasomes and its associated factors, thus reducing immunopathological response in the host. This review describes the molecular mechanism of the NLRP3 inflammasome activation in the alveoli during <i>M. tuberculosis</i> infection. Furthermore, the mechanisms of inflammasome inhibition using medicinal plant and their derivatives will also be explored, thus offering a novel perspective on the alternative control strategies of <i>M. tuberculosis</i>-induced immunopathology.