| Lepeophtheirus salmonis is an ectoparasitic copepod that causes serious disease in wild and farmed salmonids. As the relationship between L. salmonis and its hosts is not well understood, this study was undertaken to investigate whether L. salmonis immunomodulation of Atlantic salmon (Salmo salar) occurs. The presence of prostaglandin E2 (PGE2), a potent vasodilator, was identified in the secretions/excretions (SEPs) of L. salmonis at similar concentrations to that found in the saliva of other arthropod parasites. Prostaglandin E2, at physiologically relevant concentrations, inhibited lipopolysaccharide (LPS)-induced expression of numerous immune-related genes in a salmonid macrophage-like cell line.; The presence of other immunomodulatory compounds in the SEPs of these parasites was investigated. Peptides identified from SEP fractions demonstrated significant similarity to six L. salmonis expressed sequence tags (ESTs), including trypsin. Many of these ESTs showed increased expression during attached and feeding stages of the parasite. Fractions with and without PGE2 or trypsin inhibited LPS-induced expression of interleukin-1beta (IL-1beta).; In chapter 5.0, it was investigated whether a low-level L. salmonis infection, in the absence of stress response, affected expression of Atlantic salmon immune-related genes. During low-level infection, head kidney tissue expression of IL-1beta and Major histocompatibility (MH) class II increased, while MH class I expression decreased, in infected fish as compared to uninfected fish. Lipopolysaccharide stimulation of macrophages from infected fish did not further increase levels of MH class I and cyclooxygenase-2 (COX-2) expression.; To determine the effects of successive infections of L. salmonis on the immunological status of Atlantic salmon a low-level initial infection was carried out 14 d prior to a second infection. The expression of nearly all immune-related genes studied increased following initial infection with L. salmonis. However, immunological stimulation did not reduce parasite numbers or provide greater protection against a successive infection. This initial increase in expression of pro-inflammatory genes in infected fish, returned to control levels following re-infection, but was observed to increase late in the infection alongside plasma cortisol and PGE 2 levels. |
