Immunology research update from www.immunopaedia.org.za
Mycobacterium tuberculosis (Mtb), an extremely clever and tough bacterium that causes the disease tuberculosis (TB), may have a potential weakness that we may be able to exploit as we combat the disease (read more: Immunity to TB).
Beites, et al., have investigated the function and role of an Mtb enzyme that has never been studied in detail. They reported that the enzyme is essential for Mtb’s breakdown of free fatty acids which in turn lead to energy generation and the molecular building blocks for growth and survival. EtfDMtb, the enzyme reported and its deletion lead to the complete reduction of Mtb infection in mice.
This enzyme may be used as a potential drug target for the treatment of TB. Through silencing of the enzyme, it not only inhibits Mtb but also has a detrimental and toxic effect on the mycobacterium.
Through observations of Mtb proteins, the researchers found that two closely resemble two human metabolic enzymes called ETF-α and ETF-β. The latter are known to be involved in the metabolism of fatty acids, and their mutation can cause metabolic disease. Beites, et al., discovered two Mtb proteins, EtfAMtb and EtfBMtb, which together form an enzyme that works won conjunction with EtfDMtb, to carry out a similar metabolic function for Mtb i.e. beta oxidation of fatty acids.
Mtb remains a serious global public health threat and has proven to be an incredibly resilient pathogen which grows slowly and evades the immune system within the immune system itself. It is possible to cure Mtb infection with antibiotics, however it requires a lengthy treatment regimen which often is unsuccessful due to a patients inability to complete the course for several reasons. This being said, multi-drug-resistant Mtb strains have become a major medical problem in many parts of the world, and there is an urgent need for new methods of treating and fighting this pathogen. This present study by present one possible solution.
Journal article: Beites, T., et al., 2021. Multiple acyl-CoA dehydrogenase deficiency kills Mycobacterium tuberculosis in vitro and during infection. Nature Communications.