Event Abstract Back to Event In ovo elevated oocyte cortisol content induces innate immune responses in rainbow trout (Oncorhynchus mykiss) early embryonic cells Mao Li1*, Spencer Russell2, John S. Lumsden2 and John F. Leatherland1 1 University of Guelph, Biomedical Sciences, Canada 2 University of Guelph, Pathobiology, Canada In most fish embryos, the functional acquired immunity begins after hatch (1), and the protection of the embryos relies on the innate immunity of early embryo cells (1, 2). The immune suppressive effects of cortisol are well established in the developed organism, but the effects of maternal cortisol on early embryo immunity, and the ontogeny of innate immune components are not well established (2, 3). Lectins and TLRs were studied because they are widely distributed among fish tissues, and responsive to pathogens (5, 6). Naturally-ovulated rainbow trout oocytes were incubated in cortisol-enriched ovarian fluid for 3-h to examine the effects of the cortisol exposure on the ontogeny of innate immunity in rainbow trout embryos. Egg cortisol content was elevated from 4 ng/oocyte (controls - CC) to 5 (C1) and 7.5 ng/oocyte (C2) prior to fertilization (4). Lysozyme activity, intelectin, TLR-5M and TLR-5S gene expression were measured, and the intelectin and ladderlectin localization was examined in embryos using immunohistological [IH] methods. Lysozyme activity was significantly elevated in the C2 treatment group from the zygote until 13-days post fertilization (dpf), but was not affected at 21-dpf. Both intelectin and ladderlectin were present in 12-hours post-fertilization (hpf) (2-cell stage) embryos. But they had differences in response to cortisol exposure, intelectin levels (intensity of staining signal) were elevated in both cortisol treatment groups at 12-hpf and then suppressed between 36- and 48-hpf; ladderlectin was suppressed by both elevated cortisol treatments until 36-hpf compared to controls. Both lectins were distributed cell membranes and among epithelial tissues and brain tissues in late stage embryos. Intelectin mRNA was detected in oocytes and transcript levels were significantly elevated in both cortisol treatment groups relative to the controls after the 3-h incubation. There were no differences among the three treatment groups at 1- and 5-dpf, but intelectin mRNA levels were lower in the cortisol treatment groups at 13-dpf, and the transcript levels in the C2 treatment group were lower than in the CC and C1 treatment groups at 26-dpf. mRNA transcripts for the two TLR-5 genes were present in oocytes; transcript levels were significantly higher in both cortisol treatment groups relative to the controls after the 3 h incubation; TLR-5S mRNA was more abundant than that of TLR-5M mRNA. In conclusion, the ontogeny of the gene expression patterns, and the genes, lectins and lysozyme are response to increased oocyte cortisol content which indicates the importance of innate immunity in the early embryonic cells and embryo development prior to acquired immunity functions in fish. (Supported by NSERC and OMAF to JFL and JSL; NSERC Doctoral Scholarship to ML). References 1. Zapata et al. 2006. Ontogeny of the immune system of fish. Fish Shellfish Immunol. 20, 126-136; 2. Trede, et al. 2004. The use of zebrafish to understand immunity. Immunity. 20, 367-379; 3. Kindt et al. 2007. Kuby Immunology. W. H. Freeman and Co., New York, NY; 4. Li et al. 2010. The actions of cortisol in ovo on egg fertility, embryo development and growth performance of juvenile rainbow trout. Mol. Reprod. Dev. 77, 922-931; 5. Russell et al. 2008. Identification, Cloning and tissue localization of a rainbow trout (Oncorhynchus mykiss) interlectin-like protein that binds bacteria and chitin.Fish Shellfish Immunol. 25, 91-105; 6. Beutler. 2009. TLRs and innate immunity. Blood 113, 1399-1407. Keywords: cortisol, Embryo development, embryonic cell, innate immunity, ontology, rainbow trout Conference: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology, Ann Arbor, United States, 13 Jul - 16 Jul, 2011. Presentation Type: Poster Topic: Developmental endocrinology Citation: Li M, Russell S, Lumsden JS and Leatherland JF (2011). In ovo elevated oocyte cortisol content induces innate immune responses in rainbow trout (Oncorhynchus mykiss) early embryonic cells. Front. Endocrinol. Conference Abstract: NASCE 2011: The inaugural meeting of the North American Society for Comparative Endocrinology. doi: 10.3389/conf.fendo.2011.04.00098 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 22 Jul 2011; Published Online: 09 Aug 2011. * Correspondence: Dr. Mao Li, University of Guelph, Biomedical Sciences, Guelph, Ontario, N1G 2W1, Canada, mao@uoguelph.ca Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Mao Li Spencer Russell John S Lumsden John F Leatherland Google Mao Li Spencer Russell John S Lumsden John F Leatherland Google Scholar Mao Li Spencer Russell John S Lumsden John F Leatherland PubMed Mao Li Spencer Russell John S Lumsden John F Leatherland Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.
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