%0 Journal Article
%T Lipid Droplets and Mycobacterium leprae Infection
%A Ayssar A. Elamin
%A Matthias Stehr
%A Mahavir Singh
%J Journal of Pathogens
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/361374
%X Leprosy is a chronic infectious disease and is a major source of morbidity in developing countries. Leprosy is caused by the obligate intracellular bacterium Mycobacterium leprae, which infects as primary target Schwann cells. Lepromatous leprosy exhibits multiple lesions of the skin, eyes, nerves, and lymph nodes. The sites of infection are characterized by the presence of foamy macrophages, fully packed with lipid droplets (LDs), which are induced by M. leprae. In the last years, it has become evident that M. tuberculosis imports lipids from foamy macrophages and is dependent on fatty acids for growth in infected macrophages. M. leprae seems to have similar mechanisms for scavenging lipids from the host. But due to the inability to culture M. leprae on laboratory media, research progresses only slowly. However, in the last years, substantial progress has been made in the field of lipid metabolism in M. leprae. Herein, we will present and summarize the lipid droplets formation and the metabolism of lipids during M. leprae infection. 1. Introduction Leprosy, a major source of morbidity in developing countries, is a chronic infectious disease caused by the obligate intracellular bacterium Mycobacterium leprae [1, 2]. According to the system of classification of Ridley and Jopling (1966), leprosy patients show two major manifestations of the disease, designated as lepromatous leprosy (LL) and tuberculoid leprosy (TT) [1]. TT is observed in patients with good T-cell mediated (Th1) immunity and is characterized by granuloma formation and death of Schwann cells (SCs) leading to loss of myelin sheath and nerve destruction [3, 4]. TT shows only£¿few£¿lesions, and bacilli£¿can£¿rarely£¿be£¿identified. Patients with poor T-cell mediated immunity show the lepromatous-type leprosy (LL). LL leads to massive bacterial load inside host cells specially SCs and macrophages [3, 5¨C7]. The lesions of TT and LL types are named as T-lep and L-lep lesions, respectively, but damage of the nerves is observed in most of the cases of both types [7]. Lepromatous leprosy exhibits multiple lesions of the skin, eyes, nerves, and lymph nodes, which are characterized by tumor-like accumulations of foamy macrophages. The foamy macrophages are fully packed with lipid droplets (LDs) and contain high numbers of lepra bacilli. These aggregations of foamy macrophages expand slowly and disfigure the body of the host [8]. Foamy macrophages were described first by the pathologist Rudolph Virchow [9] and despite these lipid-laden cells are a hallmark of lepromatous leprosy, only recently a few
%U http://www.hindawi.com/journals/jpath/2012/361374/