Tuberculosis is a very prevalent infectious disease affecting millions of people worldwide yearly. Tuberculosis is caused by its namesake bacteria, Mycobacterium tuberculosis, which like many pathogens has developed means to protect itself from its host's immune system. M. tuberculosis is known to protect itself from degradation by macrophages, immune cells that are able to engulf harmful bacteria and pathogens that have invaded our body , but how it is able to do this remains unclear. Sethi et al.  aimed to address this question by focusing on the product of the lprI gene.
Based on computational modeling, Sethi et al. found that the predicted protein product of the lprI gene was expected to be a lipoprotein (a protein with lipid components) that was able to bind the enzyme lysozme. Lysozyme is secreted by certain immune cells, such as neutrophils and macrophages, and is ble to degrade the bacterial cell wall. Due to its expected ability to bind lysozmes, LprI was postulated to infer protection to M. tuberlculosis when it is in the intercellular space. The researchers tested this by inserting the lprI gene into M. smegmatis, a non-pathogenic Mycobacterium species, and applying hens egg white lysozme (HEWL) to the transgenic M. smegmatis. The researchers found that the addition of lprI to M. smegmatis protected it from HEWL, which under normal conditions would have degraded the cell wall. Through stoichiometric experiments they determined that LprI conferred protection by binding HEWL in a 1:1 ratio, leading to its complete inhibition. Additionally, the researchers found that LprI helped induced phagocytosis of M. smegmatis, which further protects the bacteria from cell wall degradation by removing them from the environment where lysozymes are prevalent.
Through their work Sethi et al. determined the role of the lprI gene of M. tuberculosis, which had previously not been characterized. In doing so they found that this gene conferred protection for the bacteria against intercellular lysozymes, and as such would help the pathogenicity of M. tuberculosis. LprI may represent a future therapeutic target in combating tuberculosis, as its inhibition would help infected individuals immune systems more competently deal with M. tuberculosis infections.
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 Sethi D, Mahajan S, Singh C, Lama A, Hade MD, Gupta P, Dikshit KL. Lipoprotein, LprI of Mycobacterium tuberculosis acts as a lysozyme inhibitor. J Biol Chem, 2015. [Epub ahead of print].