Possible mechanisms of host resistance to Haemonchus contortus infection in sheep breeds native to the Canary Islands

• DOI: 10.1038/srep26200
• Publication Date: 2016-05-21T09:15:31Z
• Authors: Zhengyu Guo; Jorge Francisco G...; Julia N. Hernandez; Tom N. McNeilly; Yolanda Corripio-...; David Frew; Tyler Morrison; Peng Yu; Robert W. Li
• Keywords: 0301 basic medicine; Identification; Quantitative Trait Loci; Sheep Diseases; Amphiregulin; Red Maasai; Article; Parasite Load; 03 medical and health sciences; Helminth; Animals; Disease Resistance; Inflammation; 2. Zero hunger; Mucous Membrane; Sheep; 240108 Genética animal; Sequence Analysis, RNA; Parasite Resistance; Abomasum; Gene Expression Profiling; Immunity; Gastrointestinal Nematodes; Immunity, Innate; 3. Good health; Dorper Sheep; 310902 Genética; Spain; Host-Pathogen Interactions; Haemonchus; Haemonchiasis

AbstractHaemonchus contortusappears to be the most economically important helminth parasite for small ruminant production in many regions of the world. The two sheep breeds native to the Canary Islands display distinctly different resistant phenotypes under both natural and experimental infections. Canaria Hair Breed (CHB) tends to have significantly lower worm burden and delayed and reduced egg production than the susceptible Canaria Sheep (CS). To understand molecular mechanisms underlying host resistance, we compared the abomasal mucosal transcriptome of the two breeds in response toHaemonchusinfection using RNAseq technology. The transcript abundance of 711 and 50 genes were significantly impacted by infection in CHB and CS, respectively (false discovery rate <0.05) while 27 of these genes were significantly affected in both breeds. Likewise, 477 and 16 Gene Ontology (GO) terms were significantly enriched in CHB and CS, respectively (P < 1.0 × 10−4). A broad range of mechanisms have evolved in resistant CHB to provide protection against the parasite. Our findings suggest that readily inducible acute inflammatory responses, complement activation, accelerated cell proliferation and subsequent tissue repair and immunity directed against parasite fecundity all contributed to the development of host resistance to parasitic infection in the resistant breed.