Immunohistochemical detection of Lp25 and LipL32 proteins in skeletal and cardiac muscles of fatal human leptospirosis

• Autor(a) principal: Iglezias, Silvia D’Andretta
• Data de Publicação: 2020
• Outros Autores: Abreu, Patrícia Antonia Estima, Kanamura, Cristina, Magaldi, Antonio José, Seguro, Antonio Carlos, Brito, Thales De
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Revista do Instituto de Medicina Tropical de São Paulo
• Texto Completo: https://www.revistas.usp.br/rimtsp/article/view/181206
• topic: Leptospira; Leptospirosis; Rhabdomyolysis; Weil’s disease; Lp25; LipL32

Leptospirosis is an acute infection caused by pathogenic species of the genus Leptospira, which affects humans and animals in all world. In severe forms of the disease, kidneys, liver and lungs are the main affected organs, resulting in acute kidney injury, jaundice and pulmonary hemorrhage. Previous post-mortem studies have shown that lesions are not limited to these organs. Cardiac and striated muscle injuries have already been reported, but the pathophysiology of cardiac and skeletal lesions in leptospirosis is not fully understood. It has been suggested that the tissue damage observed in leptospirosis could be directly mediated by leptospires or by their toxic cellular components. LipL32 and Lp25 are leptospira membrane proteins with unknown functions, that are present only in pathogenic strains of Leptospira spp. Both proteins induce skeletal muscle lesions similar to those observed when normal guinea pigs are inoculated with leptospires. Through immunohistochemistry, this study showed the presence of LipL32 and Lp25 proteins on muscle cell membranes and in the underlying cytoplasm of skeletal muscles, as well as focal lesions in cardiac tissues of fatal cases of leptospirosis. Altogether, these results reinforce that both proteins can be important factors in the pathogenesis of leptospirosis.