dPRLR causes differences in immune responses between early and late feathering chickens after ALV-J infection

0301 basic medicine Receptors, Prolactin Epidemiology Veterinary medicine Immunology Transgene Expression immune response 03 medical and health sciences Endocrinology Biochemistry, Genetics and Molecular Biology SF600-1100 Health Sciences dPRLR Genetics Animals Biology Internal medicine Poultry Diseases Antibody Immunology and Microbiology 2. Zero hunger 0303 health sciences Avian Leukosis Virus early feathering chickens FOS: Clinical medicine Immunity Life Sciences Hormone Prolactin 3. Good health Herpesviruses: Epidemiology, Pathogenesis, and Management Immune system Avian Leukosis Immunoglobulin M Growth Hormone Immunoglobulin G FOS: Biological sciences Medicine ALV-J Gene Therapy Techniques and Applications Chickens Spleen late feathering chickens Research Article Natural Killer Cells in Immunity
DOI: 10.1186/s13567-021-01016-7 Publication Date: 2022-01-08T20:02:42Z
ABSTRACT
AbstractTo understand the differences in immune responses between early feathering (EF) and late feathering (LF) chickens after infection with avian leukosis virus, subgroup J (ALV-J), we monitored the levels of prolactin, growth hormone and the immunoglobulins IgG and IgM in the serum of LF and EF chickens for 8 weeks. Moreover, we analysed the expression of immune-related genes in the spleen and the expression of PRLR, SPEF2 and dPRLR in the immune organs and DF-1 cells by qRT–PCR. The results showed that ALV-J infection affected the expression of prolactin, growth hormone, IgG and IgM in the serum. Regardless of whether LF and EF chickens were infected with ALV-J, the serum levels of the two hormones and two immunoglobulins in EF chickens were higher than those in LF chickens (P  < 0.05). However, the expression of immune-related genes in the spleen of positive LF chickens was higher than that in the spleen of positive EF chickens. In the four immune organs, PRLR and SPEF2 expression was also higher in LF chickens than in EF chickens. Furthermore, the dPRLR expression of positive LF chickens was higher than that of negative LF chickens. After infection with ALV-J, the expression of PRLR in DF-1 cells significantly increased. In addition, overexpression of PRLR or dPRLR in DF-1 cells promoted replication of ALV-J. These results suggested that the susceptibility of LF chickens to ALV-J might be induced by dPRLR.
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