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ABSTRACT
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.
GRAPHICAL ABSTRACT
Abbreviations
| M.leprae | = | Mycobacterium leprae |
| M. tuberculosis | = | Mycobacterium tuberculosis |
| WHO | = | World Health Organization |
| G2D | = | Grade-2 disability |
| LL | = | lepromatous leprosy |
| BT | = | borderline tuberculoid leprosy |
| BB | = | mid-borderline leprosy |
| BL | = | borderline lepromatous leprosy |
| TT | = | tuberculoid leprosy |
| ENL | = | erythema nodosum leprosum |
| PEP | = | post-exposure prophylaxis |
| SDR | = | single dose of rifampicin |
| PGL-I | = | phenolic glycolipid I |
| MDT | = | multidrug therapy |
| TLRs | = | Toll-like receptors |
| IFN-γ | = | interferon-γ |
| TNF-α | = | tumour necrosis factor-α |
| iNOS | = | inducible nitric oxide synthase |
| NOD | = | nucleotide-binding oligomerization domain |
| NLRs | = | NOD-like receptors |
| TGF | = | transforming growth factor |
| JAG1 | = | protein jagged 1 |
| Hlp | = | histone-like protein |
| SNPs | = | single nucleotide polymorphisms |
| MAC | = | membrane attack complex |
| LAM | = | lipoarabinomannan |
| LM | = | lipomannan |
| PG | = | peptidoglycan |
| AG | = | arabinogalactan |
| PDIMs | = | phthiocerol dimycocerosate |
| TMM | = | trehalose mono-mycolate |
| DAP | = | diaminopimelic acid |
| TAG | = | triacylglycerol |
| GPAT | = | glycerol-3-phosphate acyltransferase |
| LDs | = | Lipid droplets |
| ADRP | = | adipose differentiation-related protein |
| PPARs | = | peroxisome proliferator-activated receptors |
Acknowledgments
The authors wish to thank Eri Kawakami and Sumie Sadakata for their invaluable assistance. The authors also wish to thank Dr. Norihisa Ishii for the courtesy of providing the histopathological photograph.
Disclosure statement
No potential conflict of interest was reported by the author(s).