Signatures of resistance to Lepeophtheirus salmonis include a TH2-type response at the louse-salmon interface

Disease outbreaks with the salmon louse Lepeophtheirus salmonis cause significant economic losses in mariculture operations worldwide. Variable innate immune responses at the louse-attachment site contribute to differences in susceptibility among species such that members of Salmo spp. are more susceptible to infection than those of some Oncorhynchus spp. Relatively little is known about the mechanisms that contribute to disease resistance or susceptibility to L. salmonis in salmon. Here, we utilize histochemistry and transcriptomics in a comparative infection model with susceptible (Atlantic, sockeye) and resistant (coho) salmon. At least three cell populations (MHII beta+, IL1 beta+, TNF alpha+) were activated in coho salmon skin during L. salmonis infection. Locally elevated expression of several pro-inflammatory mediators (e.g. IL1 beta, IL8, TNF alpha, COX2, C/EBP beta), and tissue repair enzymes (MMP9, MMP13) were detected in susceptible and resistant species. However, responses specific to coho salmon (e.g. 1L4, 1L6, TGF beta) or responses shared among susceptible salmon (e.g. SAP, TRF, Cath in Atlantic and sockeye salmon) provide evidence for speciesspecific pathways contributing to resistance or susceptibility, respectively. Our results confirm the importance of an early pro-inflammatory T(H)1 -type pathway as an initial host response during infection with Pacific sea lice, and demonstrate subsequent regulatory T(H)2-type processes as candidate defense mechanisms in the skin of resistant coho salmon. Crown Copyright (C) 2014 Published by Elsevier Ltd. All rights reserved.