Abstract

In experimental autoimmune hepatitis (EAH) of Th1 profile, an extract of adult Ascaris suum worms (ASC) was previously found to deviate the immune response to a Th2/IL-10 pattern. Here, the effects of treatment with ASC on production of TGF-β and the anti-Ascaris isotypes IgG1 and IgG2a in EAH were evaluated. EAH was induced in BALB/c mice, intravenously with concanavalin A. Two hours later, these animals received ASC (EAH+ASC group) or PBS vehicle (EAH group). IgG1 and IgG2a were evaluated 8 h, 24 h and 7 d after induction. TGF-β was measured in a splenocyte culture at this last time. The isotype levels in the EAH group were low throughout the kinetics. In the EAH+ASC group, there was significant production of IgG1 at 24 h and 7 d, but of IgG2a only at 7 d. There was statistically greater production of TGF-β in the EAH+ASC group. The higher levels of IgG1 and TGF-β in this group suggest that an additional Th1 response control route exists in EAH, which needs to be investigated.

Highlights

  • An extract of adult Ascaris suum worms (ASC) has been found to suppress the inflammatory response to heterologous antigens through mechanisms that depend on IL-10/TGF-β and CD4+CD25+Foxp3+ T cells (Araújo et al, 2010; Souza et al, 2002)

  • In the experimental autoimmune hepatitis (EAH)+ASC group, production of IgG2a only occurred at the 7th day and was at higher levels than in the EAH group

  • Regarding anti-Ascaris IgG1, production occurred at 8 h, 24 h and the 7th day, but was significantly greater at the latter two times (Figure 1A), in relation to EAH group

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Summary

Introduction

An extract of adult Ascaris suum worms (ASC) has been found to suppress the inflammatory response to heterologous antigens through mechanisms that depend on IL-10/TGF-β and CD4+CD25+Foxp3+ T cells (Araújo et al, 2010; Souza et al, 2002). The levels of TGF-β and anti-Ascaris IgG isotypes in this inflammation model were not evaluated. Immunization with PAS-1, a protein of A. suum, stimulated the Th2 response, production of IL-10 and TGF-β in allergic airway inflammation induced by OVA in mice (Araújo et al, 2010). It is known that treatment with ASC causes negative modulation of immunopathology in EAH, with development of an immune response of Th2 profile, evaluation of other modulation routes becomes necessary

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