02202nas a2200289 4500000000100000008004100001260001200042653001200054653002500066653001700091653002200108653001500130653001500145100002200160700001500182700001600197700001300213700001500226700001500241700001300256245005600269856008100325300001400406490000700420520147100427022001401898 2022 d c12/202210aleprosy10aMycobacterium leprae10aSchwann cell10alipids metabolism10aMacrophage10aPseudogene1 aSugawara-Mikami M1 aTanigawa K1 aKawashima A1 aKiriya M1 aNakamura Y1 aFujiwara Y1 aSuzuki K00aPathogenicity and virulence of Mycobacterium leprae uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9635560/pdf/KVIR_13_2141987.pdf a1985-20110 v133 a
Leprosy is caused by Mycobacterium leprae (M. leprae) and M. lepromatosis, an obligate intracellular organism, and over 200,000 new cases occur every year. M. leprae parasitizes histiocytes (skin macrophages) and Schwann cells in the peripheral nerves. Although leprosy can be treated by multidrug therapy, some patients relapse or have a prolonged clinical course and/or experience leprosy reaction. These varying outcomes depend on host factors such as immune responses against bacterial components that determine a range of symptoms. To understand these host responses, knowledge of the mechanisms by which M. leprae parasitizes host cells is important. This article describes the characteristics of leprosy through bacteriology, genetics, epidemiology, immunology, animal models, routes of infection, and clinical findings. It also discusses recent diagnostic methods, treatment, and measures according to the World Health Organization (WHO), including prevention. Recently, the antibacterial activities of anti-hyperlipidaemia agents against other pathogens, such as M. tuberculosis and Staphylococcus aureus have been investigated. Our laboratory has been focused on the metabolism of lipids which constitute the cell wall of M. leprae. Our findings may be useful for the development of future treatments.
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