Abstract
Activation of complement by Taenia taeniaeformis larvae was examined by immunohistochemical staining of liver sections from resistant BALB/cByJ mice, moderately susceptible C3H/HeJ mice, and susceptible C3H/HeDub mice. C3 deposition was found on larval surfaces as early as 2 days post-infection, the earliest period of examination, and persisted in all three strains of mice until day 6 post-infection when it was no longer present. Additionally, oncospheres activated in vitro demonstrated complement binding activity when exposed to non-immune mouse sera from all three strains. The alternative pathway was implicated by the inability to inhibit the activation of C3 on oncospheres with serum treated with EGTA and Mg 2+ , the failure to detect IgM or IgG on larval surfaces in situ , and the inability to detect by ELISA circulating antibody to a solubilized T. taeniaeformis oncosphere extract prior to 6 days post-infection. Administration of anti-complementary cobra venom factor to mice prior to oral infection resulted in decreased parasite mortality, particularly in the normally resistant BALB/cByJ strain. It is suggested that the role of complement in innate resistance is an indirect action involving host cell recognition and/or activation rather than a direct lytic effect
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have