Expression of antibodies directed to paracoccidioides brasiliensis glycosphingolipids during the course of paracoccidioidomycosis trea...

• Grant number: 07/01049-2
• Support Opportunities: Regular Research Grants - Publications - Scientific article
• Start date: May 01, 2007
• End date: May 31, 2007
• Field of knowledge: Biological Sciences - Immunology - Immunochemistry
• Principal Investigator: Anita Hilda Straus Takahashi
• Grantee: Anita Hilda Straus Takahashi
• Host Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

Paracoccidioidomycosis (PCM) is a granulomatous disease caused by the dimorphic fungus Paracoccidioides brasiliensis. The immunoglobulin classes and isotypes of antibodies directed to acidic glycosphingolipids (GSLs) and glucosylceramide of P. brasiliensis were determined by ELISA for sera from 31 PCM patients. The reactivity of 38 serum sample was analyzed considering the stage of treatment: before antifungal treatment (BT, N=10), during 1-4 months treatment (T1-4, N=9), during 5-12 months treatment (T5-12, N=9), and post-treatment (PT, N=10), being seven serum samples from same patients at different stages of treatment. Sera from normal subjects (N=12) were used as control. Only the GSL antigen Pb-1, which presents carbohydrate structure Galfb1-6(Mana1-3)Manb1, was reactive with PCM patient sera. PCM sera did not react with Pb-2, which lacks Galf residue and is considered the biosynthetic precursor of Pb-1, indicating that Galf residue is essential for antibody reactivity. Pb-1 glycolipid, in non-treated patients, elicited a primary immune response with IgM production, and subsequent switching to IgG1 production. IgG1 titer increased after the start of antifungal treatment (T1-4 group), and a general decrease of anti-Pb-1 antibody titers was observed after 5 months of treatment (T5-12 and PT groups). Pb-1 antigen, an acidic GSL with terminal Galf residue, has potential application as elicitors of host immune response in PCM. (AU)