11 research outputs found

    Specific Humoral Immunity versus Polyclonal B Cell Activation in Trypanosoma cruzi Infection of Susceptible and Resistant Mice

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    Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, affects 10–12 million people in Latin America. Patent parasitemia develops during acute disease. During this phase, polyclonal B cell activation has been reported to generate high levels of serum antibody with low parasite specificity, and delayed protective humoral immunity, which is necessary to prevent the host from succumbing to infection. In this manuscript, data show that relatively resistant mice have improved parasite-specific humoral immunity and decreased polyclonal B cell activation compared to susceptible mice. Parasite-specific humoral immunity was associated with differential expansion of B cell subsets and T cells in the spleen, as well as with increased Th1 and decreased Th2 cytokine production. These data suggest that host susceptibility/genetic biases impact the development of humoral responses to infection. Th2 cytokines are generally associated with improved antibody responses. In the context of T. cruzi infection of susceptible mice, Th2 cytokines were associated with increased total antibody production concomitant with delayed pathogen-specific humoral immunity. This study highlights the need to consider the effect of host biases when investigating humoral immunity to any pathogen that has reported polyclonal B cell activation during infection

    Haemolytic fungi isolated from sago starch in Papua New Guinea

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    Sago haemolytic disease (SHD) is a rare but often fatal illness linked to consumption of stale sago starch in Papua New Guinea. Although the aetiology of SHD remains unknown, mycotoxins are suspected. This study investigated whether fungi isolated from Papua New Guinean sago starch were haemolytic. Filamentous fungi and yeasts from sago starch were grown on sheep blood agar and some on human blood agar. Clear haemolytic activity was demonstrated by 55% of filamentous fungal isolates, but not by yeasts. A semi-quantitative bioassay was developed involving incubation of human erythrocytes with fungal extracts. Extracts of cultures of Penicillium, Aspergillus and Fusarium all caused rapid haemolysis in the bioassay. Partial fractionation of extracts suggested that both polar and non-polar haemolytic components had haemolytic activity in vitro. Further work is warranted to identify these metabolites and determine if they play a role in SHD

    Tissue Damage Caused by the Direct and Indirect Action of Complement

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