Article
Arginase I, polyamine, and prostaglandin E2 pathways suppress the inflammatory response and contribute to diffuse cutaneous leishmaniasis
Registro en:
COSTA, J. F. et al. Arginase I, polyamine, and prostaglandin E2 pathways suppress the inflammatory response and contribute to diffuse cutaneous leishmaniasis. Journal of Infectious Diseases, v. 211, n. 3, p. 426-435, 2015.
1537-6613
10.1093/infdis/jiu455
Autor
Costa, Jaqueline França
Van Weyenbergh, Johan Jozef Rosa Maria
Boaventura, Viviane Sampaio
Luz, Nívea Farias
Santos, Hayna Malta
Oliveira, Murilo Cezar Souza
Campos, Daniela Conceição Santos de
Saldanha, Ana Cristina
dosSantos, Washington Luis Conrado
Bozza, Patrícia Torres
Barral Netto, Manoel
Barral, Aldina Maria Prado
Costa, Jackson Mauricio Lopes
Borges, Valeria de Matos
Resumen
Diffuse cutaneous leishmaniasis (DCL) is a rare clinical manifestation of tegumentary leishmaniasis. The molecular
mechanisms underlying DCL pathogenesis remain unclear, and there is no efficient treatment available.
This study investigated the systemic and in situ expression of the inflammatory response that might contribute
to suppression in DCL. The plasma levels of arginase I, ornithine decarboxylase (ODC), transforming growth
factor β (TGF-β), and prostaglandin E2 (PGE2) were higher in patients with DCL, compared with patients with
localized cutaneous leishmaniasis (LCL) or with controls from an area of endemicity. In situ transcriptomic
analyses reinforced the association between arginase I expression and enzymes involved in prostaglandin and
polyamine synthesis. Immunohistochemistry confirmed that arginase I, ODC, and cyclooxygenase2 expression
was higher in lesion biopsy specimens from patients with DCL than in those from patients with LCL. Inhibition
of arginase I or ODC abrogates L. amazonensis replication in infected human macrophages. Our data implicate
arginase I, ODC, PGE2, and TGF-β in the failure to mount an efficient immune response and suggest perspectives
in the development of new strategies for therapeutic intervention for patients with DCL.
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