The immune response of carp to Trypanoplasma borreli: kinetics of immune gene expression and polyclonal lymphocyte activation.

Although Trypanoplasma borreli induces the production of non-specific antibodies, survival of infection is associated with the production of T. borreli specific antibodies, able to lyse this parasite in the presence of complement. During the lag phase of this acquired immune response, innate immune mechanisms must limit multiplication of T. borreli. A heat-labile fraction of T. borreli together with CpG motifs in the DNA of this parasite are responsible for the induction of nitric oxide (NO) and probably also for the induction of expression of the inflammatory cytokines tumor necrosis factor (TNF)alpha and interleukin (IL)-1beta by carp phagocytes in vitro. In the signal transduction pathway leading to activation of phagocytes, protein tyrosine kinase and protein kinase C are involved and probably collaborate in activation of the transcription factor nuclear factor (NF)-kappaB. In vivo, carp intraperitoneally injected with T. borreli up-regulate expression of TNFalpha, IL-1beta and mRNAs for acute phase response proteins (complement factor 3, serum amyloid A and alpha-2-macroglobulin).