Contribution of C5-mediated mechanisms to host defence against Echinococcus granulosus hydatid infection

The aim of this work was to investigate the contribution of complement C5-m ediated mechanisms, with an emphasis on inflammation, to host defences agai nst Echinococcus granulosus hydatid disease. Thus, Mle compared the systemi c and local inflammatory responses induced by the parasite, and the outcome of infection, between congenic C5-sufficient (B10.D2 n/SnJ) and C5-deficie nt (B10.D2 o/SnJ),nice challenged with protoscoleces. Indirect evidence of in-vivo complement activation during the establishment phase was obtained; infection induced serum amyloid P and eosinophil responses which were depen dent on C5. Early recruitment of polymorphonuclear cells was not dependent on the presence of C5, The higher capacity of C5-sufficient mice to recruit eosinophils was also observed during the cystic phase of infection, and mi ce recruiting more eosinophils developed lower parasite masses. Analysis of the outcome of infection after 8 months showed that C5-sufficient mice wer e more resistant to infection than C5-deficient mice in terms of individual s with no cysts; this trend was not statistically significant. In addition, C5-deficient mice developed higher numbers of large (>5 mm in diameter) cy sts and higher cyst weights than C5-sufficient mice indicating that C5-medi ated mechanisms are detrimental for parasite growth. Taken together, our re sults suggest that co,complement, through C5-mediated effectors, contribute s to host defences by both restricting the establishment of infection and c ontrolling the growth of established cysts, This contribution may, at least partially, be associated with the ability of C5a to promote eosinophil inf iltration.