Immune Defences of Teleost Fish - Aquaculture Nutrition: Gut Health, Probiotics and Prebiotics - page 16

include the antibacterial peptides (pleurocidin, piscidins, trypsin-like proteases, cathepsins
L and B, lysozyme and β-defensins), c-reactive protein (CRP), lectins (involved in carbo-
hydrate recognition, resulting in agglutination, opsonization and complement activation) and
immunoglobulins, which confer passive immunity on newly hatched fry who mucus-feed from
parental skin (Hildemann 1959; Buckley et al. 2010).
In addition to the barrier defence associated epithelial cells, the main effector cells of
the teleost innate immune system include neutrophils, monocytes, macrophages and granu-
locytes such as basophils, eosinophils, mast cells/eosinophilic granule cells (MCs/EGCs) and
rodlet cells. All of these play a role in inflammatory responses to acute or chronic infection.
The neutrophils and macrophages function as phagocytes in the recognition and clearance of
pathogenic materials, and when activated can release anti-microbials as part of the respira-
tory burst and cytokines to instruct other parts of the immune response (reviewed in Rombout
et al. 2010). Rodlet cells are thought to be immature eosinophilic granulocytes that play a
significant role in defence against parasites; rodlet cell numbers increase in the presence of
helminths where aggregations have been observed in infected epithelia of the gills and intesti-
nal tract. MCs/EGCs possess both acidophilic and basophilic granules; these cells are recruited
and observed in high numbers in chronically inflamed tissues. Degranulation results in the
secretion of acid and alkaline phosphatases, tryptase, nucleotidases, 5-HT, lysozyme and pep-
tide antibiotics (piscidins and pleurocidin). Recruitment, activation and degranulation of these
cells have been described in response to the bacterial infection of Aeromonas salmonicida ,
Renibacterium salmoninarum and nematode infestation of intestinal tissue (reviewed in Reite
and Evensen 2006).
The first step in activation of innate immune effector functions is the recognition of
pathogens and their antigens. Pathogen recognition occurs in response to a broad array of
conserved pathogen-associated molecular patterns (PAMPs) expressed by the pathogen; these
in turn are recognized by their innate counterparts, the pattern recognition receptors (PRRs).
This array of PRRs exists as both secreted and membrane-associated recognition receptors.
In general, the secreted PRRs include collectins, pentraxins, complement components and
mannose binding lectin (MBL). The membrane-associated PRRs exist as either signalling
receptors or binding receptors for clearance by phagocytosis. The secreted PRRs such as
lectins (MBL, interlectin and pentraxins) and complement components are involved in
opsonization, phagocytosis, chemotaxis, inflammation and pathogen killing. The lectin class
of molecules is involved in recognition of sugar moieties expressed by pathogens and not
normally expressed on host tissues. This class of molecules consists of the collectin MBL,
which activates complement cascades via the lectin pathway. MBL recognizes mannose,
fucose and N-acetyl-D-glucosamine, acting as an opsonin for recognition and phagocytosis
as well as activating serine proteases for proteolytic breakdown (Nakao et al. 2006). The
pentraxin molecules are composed of five identical subunits and include CRP and SAA. CRP
binds phosphocholine moieties of certain bacterial and fungal cell wall lipopolysaccharides,
resulting in the activation of the complement cascade via binding to C1q. Another class of
lectin molecule has been identified in teleost fish, namely interlectin (reviewed in Vasta et al.
2011). So far, this molecule has been demonstrated at the molecular level but functional data
have yet to ascertain a clear role for it in innate immunity; mammalian studies, however,
have indicated that this class of lectin may be important for the recognition of and responses
to bacterial cell wall galactofuranose moieties and protection against intestinal nematode
infection (Tsuji et al. 2001; Pemberton et al. 2004). Finally, the last group of secreted PRRs