glycoinositolphospholipids from leishmania braziliensis and l. infantum modulation of innate immune system and variations in carbohydrate structure从利什曼虫glycoinositolphospholipids braziliensis和l . infantum调制的先天免疫系统和碳水化合物结构的变化.pdfVIP

glycoinositolphospholipids from leishmania braziliensis and l. infantum modulation of innate immune system and variations in carbohydrate structure从利什曼虫glycoinositolphospholipids braziliensis和l . infantum调制的先天免疫系统和碳水化合物结构的变化.pdf

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glycoinositolphospholipids from leishmania braziliensis and l. infantum modulation of innate immune system and variations in carbohydrate structure从利什曼虫glycoinositolphospholipids braziliensis和l . infantum调制的先天免疫系统和碳水化合物结构的变化

Glycoinositolphospholipids from Leishmania braziliensis and L. infantum: Modulation of Innate Immune System and Variations in Carbohydrate Structure 1,2 1 ´ 2 3 Rafael Ramiro Assis , Izabela Coimbra Ibraim , Fatima Soares Noronha , Salvatore Joseph Turco , Rodrigo Pedro Soares1* ´ ˜ 1 Centro de Pesquisas Rene Rachou, Fundac¸ao Oswaldo Cruz - FIOCRUZ, Belo Horizonte, Brazil, 2 Departmento de Microbiologia, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil, 3 Department of Biochemistry, University of Kentucky Medical Center, Lexington, Kentucky, United States of America Abstract The essential role of the lipophosphoglycan (LPG) of Leishmania in innate immune response has been extensively reported. However, information about the role of the LPG-related glycoinositolphospholipids (GIPLs) is limited, especially with respect to the New World species of Leishmania. GIPLs are low molecular weight molecules covering the parasite surface and are similar to LPG in sharing a common lipid backbone and a glycan motif containing up to 7 sugars. Critical aspects of their structure and functions are still obscure in the interaction with the vertebrate host. In this study, we evaluated the role of those molecules in two medically important South American species Leishmania infantum and L. braziliensis, causative agents of visceral (VL) and cutaneous Leishmaniasis (CL), respectively. GIPLs derived from both species did not induce NO or TNF-a production by non-primed murine macrophages. Additionally, primed macrophages from mice (BALB/c, C57BL/6, TLR2 2/ 2 an

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