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Tuberculosis is amongst the leading causes of bacteria-related morbidity and mortality worldwide, caused by Mycobacterium tuberculosis bacterium, which attacks the lungs of infected individuals. Incidence of diphtheria – another acute infectious respiratory disease, caused by Corynebacterium diphtheriae bacterium – has declined significantly in the last century due to vigorous vaccination. However, according to CDC, 1 in 10 adults and 1 in 5 children who get diphtheria, die if infected.

Mycobacterial cell walls are special in a sense that they contain an extra layer of fatty acids, called mycolic acids, on the outer surface of the cell, forming a protective barrier resembling the outer membrane of Gram-negative bacteria. Such wall architecture allows M. tuberculosis, which is the main cause of tuberculosis in humans, as well as other related bacteria to evade the immune system and resist the majority of treatments.

Moreover, C. diphtheriae, which causes diphtheria, shares the common protective features of mycolic cell wall. Therefore, identification of the main players in the complex cell wall synthesis in Corynebacteria and Mycobacteria is bound to open up new avenues for target treatments of these diseases.

A novel study published in BMC Biology reveals a universal target for tuberculosis and diphtheria treatments, which is not only involved in biosynthesis of cell wall components, but can also influence other pathogenic features of bacteria, such as utilization of important carbon sources within the human body and response to oxidative stress.

IpsA is a transcriptional regulator conserved throughout Corynebacteria and Mycobacteria, and has been previously found to affect cell morphology. The scientists now demonstrate that disruption of ipsA gene leads to significant loss of protective lipids within the cell wall.

Moreover, ipsA mutation was shown to impair the use of important carbon sources commonly available to M. tuberculosis and C. diphtheria in the body, such as inositol, further impairing growth of these pathogens in the disease environment, and is thought to affect a range of other processes as well.

Though still at the academic phase, discovery of a wide-spectrum drug target effective in both M. tuberculosis and C. diphtheria, could become a powerful and universal treatment for life-threatening tuberculosis and diphtheria, as long as target inactivation and drug delivery options are developed and put into practice.

Source: www.technology.org