Identification of Brugia malayi adult worm molecules immunoreactive with sera of infected animals treated with antifilarial and re-infected with homologous infection and their role in the establishment of infection in Mastomys coucha

Abstract

The present study was aimed at identifying molecules of Brugia malayi adult worm (BmA) that are immunoreactive with sera of B. malayi-infected Mastomys coucha treated with albendazole (ALB) or diethylcarbamazine (DEC) and re-exposed to infection and the effect of immunization with the molecules on the establishment of infection in M. coucha. A ∼62 kDa molecule showed strong reactivity with sera of infected ALB-treated reinfected animals whereas ∼32 kDa and ∼45 kDa molecules strongly reacted with sera of DEC-treated reinfected animals. Two molecules (∼22 kDa and ∼28 kDa) reacted with sera of infected untreated and reinfected control animals. Immunization with ∼62 kDa molecules reduced the adult worm recovery by 58% (P < 0.001) and microfilaremia by 32–54% (P < 0.05–0.01) of unimmunized controls. Animals immunized with the ∼32 kDa molecule exhibited 63% recovery of adult worms with no effect on circulating microfilaraemia. L3 inoculation in ∼62 kDa-immunized animals upregulated cellular proliferation, interferon-γ (IFN-γ) and IgG responses (P < 0.001) but downregulated interleukin-10 (IL-10) response (P < 0.001). Animals immunized with ∼22, ∼28, ∼32 and ∼45 kDa molecules and bearing L3-induced infection showed mixed responses. Lymph node cells of unimmunized animals exposed to ∼28, ∼32 and ∼62 kDa molecules showed significant DNA damage (P < 0.001) as compared to untreated control; ∼62 kDa molecule induced maximum damage. In conclusion, immunization with a ∼62 kDa molecule suppressed the establishment of L3-induced infection in M. coucha and this correlated with enhanced cellular proliferation and IFN-γ release, downregulation of IL-10, increased levels and DNA damage in lymph node cells.