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Researchers analyzed the enzymes of Mycobacterium tuberculosis.
The role of this enzyme has never been studied in depth and found that fatty acids that are essential for the collapse of Mtb provide energy and molecular growth and survival building blocks
.
Merely deleting an enzyme they called EtfDMtb would make Mtb unable to sustain infection in mice
Dr.
Sabine Ehrt, professor of microbiology and immunology at Weill Cornell Medicine and senior author, said: "This enzyme is an attractive drug target for the treatment of tuberculosis-silencing it not only starves the bacteria, but also has additional toxicity to it.
Role
.
"
This new discovery comes from the observation of the first author, Dr.
Tiago Beites, a lecturer in Ehrt's laboratory
.
When analyzing the Mtb protein, Dr.
Dr.
Bates and his colleagues further studied and finally found that two Mtb proteins (they renamed them EtfAMtb and EtfBMtb) together formed an enzyme that worked in conjunction with another Mtb enzyme, which they called EtfDMtb, right Mycobacterium tuberculosis performs a similar metabolic function—especially a process related to decomposition, called fatty acid oxidation
.
Although it has always been believed that the fatty acid metabolism in Mycobacterium tuberculosis is covered by a large number of excess enzymes, making this group of pathways a poor drug target, the research team found that the three-component complex they found has an effect on Mycobacterium tuberculosis.
The normal growth and survival of humans are essential
.
A mutant Mycobacterium tuberculosis that lacks EtfDMtb cannot promote its growth through fatty acids or related cholesterol
"This is a good initial indication that inhibiting this enzyme will be an effective way to treat tuberculosis," said Dr.
Bates
.
Even in the era of antibiotics, Mycobacterium tuberculosis remains a major public health threat
.
It is estimated that it will infect nearly a quarter of the population at any time, mainly in South and Southeast Asia, China and parts of Africa
Mycobacterium tuberculosis is difficult to treat because it grows slowly and can hide inside the immune system, especially in phagocytic macrophages
But it cannot be destroyed
.
It is possible to treat Mycobacterium tuberculosis infection with antibiotics, but it requires a long-term treatment plan, which patients often cannot follow
There are about 4000 genes in the genome of Mycobacterium tuberculosis, and it also has the powerful ability to evolve treatment resistance
.
Multidrug-resistant Mycobacterium tuberculosis strains have become a major medical problem in many parts of the world, and there is an urgent need for drugs that kill this pathogen through a new mechanism
Evidence supporting the goal of fatty acid metabolism is emerging
.
Last year, an independent research team in Europe reported that certain compounds called dioxybenzopyridine-indole can kill Mycobacterium tuberculosis by inhibiting an enzyme called EtfDMtb by Dr.
The researchers also plan to conduct more studies to determine whether EtfDMtb or a closely related enzyme can be a good drug target for other pathogenic bacteria
Journal Reference :
Tiago Beites, Robert S.
Jansen, Ruojun Wang, Adrian Jinich, Kyu Y.
Rhee, Dirk Schnappinger, Sabine Ehrt.
Multiple acyl-CoA dehydrogenase deficiency kills Mycobacterium tuberculosis in vitro and during infection .
Nature Communications , 2021; 12 (1) DOI : 10.
1038/s41467-021-26941-1
