title: Oral exposure of broiler breeder hens to extra thyroxine modulates early adaptive immune responses in progeny chicks.
abstract: Based on the findings of a recent study suggesting a decreased cold-induced ascites incidence in broiler progeny from hyperthyroid (HYPER) breeder hens, and a controversy on the effects of hyperthyroidism on immunocompetence, the present study was conducted to determine the probable adverse effect of induced maternal hyperthyroidism on immune function in progeny chicks. Breeder hens (n = 88) were randomly allotted to the control or HYPER groups and received common or thyroxine (T4)-added (1 mg/L) water, respectively. The hens were artificially inseminated, and hatching eggs (n = 924) were incubated. Thereafter, the male hatchlings (n = 288) were reared for 42 d, and several cellular and humoral immune responses were evaluated at standard or low ambient temperature. Prevaccination antibody titers to Newcastle disease, infectious bronchitis, and infectious bursal disease virus were higher in HYPER chicks during 1 wk of age, although not different in their dams. For primary response to SRBC administered at 7 d of age, HYPER chicks recorded higher total, IgM (d 14), and IgG (d 21) anti-SRBC antibody titers. Higher cutaneous basophilic hypersensitivity response in HYPER chicks (d 10) was not observed at 35 d of age. Carbon clearance assay showed no difference, but in vitro lymphoproliferative response to concanavalin A was higher in 19-d-old HYPER chicks, independent of temperature treatment. An increase in lymphocyte percentage coincided with a decreased heterophil percentage and heterophil to lymphocyte ratio (d 14) in the HYPER group. The weight of lymphoid organs in progeny was not influenced by the oral exposure of dams to extra T4. Independent of T4 treatment, cold exposure was generally associated with decreased immune functions at early stages. The data suggested that oral exposure of broiler breeder hens to 1 mg/L of T4 not only had no adverse effect on immune function, but also modulated early adaptive immune responses in progeny chicks for which the causal mechanisms remain to be unraveled.
authors.affiliation: Department of Animal Science, Shiraz University, Shiraz, Iran. aakhlaghi@shirazu.ac.ir
authors.forename: A
authors.initials: A
authors.lastname: Akhlaghi
authors.forename: M J
authors.initials: MJ
authors.lastname: Zamiri
authors.forename: Y
authors.initials: Y
authors.lastname: Jafari Ahangari
authors.forename: H
authors.initials: H
authors.lastname: Atashi
authors.forename: Z
authors.initials: Z
authors.lastname: Ansari Pirsaraei
authors.forename: H
authors.initials: H
authors.lastname: Deldar
authors.forename: A N
authors.initials: AN
authors.lastname: Eghbalian
authors.forename: A A
authors.initials: AA
authors.lastname: Akhlaghi
authors.forename: B
authors.initials: B
authors.lastname: Navidshad
authors.forename: K
authors.initials: K
authors.lastname: Yussefi Kelarikolaei
authors.forename: S R
authors.initials: SR
authors.lastname: Hashemi
mesh_terms: D056704:Adaptive Immunity; D000818:Animals; D000914:Antibodies, Viral / Q000097:blood* / Q000276:immunology; D018175:Birnaviridae Infections / Q000097:blood / Q000276:immunology / Q000662:veterinary; D002645:Chickens; D018352:Coronavirus Infections / Q000097:blood / Q000276:immunology / Q000662:veterinary; D005260:Female; D006980:Hyperthyroidism / Q000139:chemically induced / Q000662:veterinary*; D007112:Immunity, Maternally-Acquired; D008297:Male; D009521:Newcastle Disease / Q000097:blood / Q000276:immunology; D011201:Poultry Diseases / Q000097:blood / Q000276:immunology*; D013974:Thyroxine / Q000008:administration & dosage*
chemical_list: D000914:Antibodies, Viral; D013974:Thyroxine