Cytokine responses to eye spray adjuvants for enhancing vaccine-induced immunity in chickens.

Eye spray influenza vaccines for chickens are increasingly available; however, how to enhance cellular and antibody responses to them remains undetermined. Here, eye-drops containing the immune-enhancing adjuvants Pam2CSK4 or polyI:C were assessed in chickens. Application of these TLR agonists to chicken conjunctiva resulted in up-regulation of IL-1ß, but not other cytokines, including IFN and IL-6, in the spleen, lung and Harderian gland. Thus, responses to adjuvant applied to the conjunctival mucosa of chickens differ from those expected from the responses to intra-nasal adjuvants in mammals. Identifying an appropriate delivery route for adjuvants is crucial for evoking immune responses in chickens.

Evolution of the DEAD box helicase family in chicken: chickens have no DHX9 ortholog.

Viral RNA represents a pattern molecule that can be recognized by RNA sensors in innate immunity. Humans and mice possess cytoplasmic DNA/RNA sensors for detecting viral replication. There are a number of DEAD (Asp-Glu-Ala-Asp; DExD/H) box-type helicases in mammals, among which retinoic acid-inducible gene 1 (RIG-I) and melanoma differentiation-associated protein 5 (MDA50) are indispensable for RNA sensing; however, they are functionally supported by a number of sensors that directly bind viral RNA or replicative RNA intermediates to convey signals to RIG-I and MDA5. Some DEAD box helicase members recognize DNA irrespective of the origin. These sensors transmit IFN-inducing signals through adaptors, including mitochondrial antiviral signaling. Viral double-stranded RNAs are reportedly sensed by the helicases DDX1, DDX21, DHX36, DHX9, DDX3, DDX41, LGP2 and DDX60, in addition to RIG-I and MDA5, and induce type I IFNs, thereby blocking viral replication. Humans and mice have all nucleic acid sensors listed here. In the RNA sensing system in chicken, it was found in the present study that most DEAD box helicases are conserved; however, DHX9 is genetically deficient in addition to reported RIG-I. Based on the current genome databases, similar DHX9 deficiency was observed in ducks and several other bird species. Because chicken, but not duck, was found to be deficient in RIG-I, the RNA-sensing system of chicken lacks RIG-I and DHX9 and is thus more fragile than that of duck or mammal. DHX9 may generally compensate for the function of RIG-I and deficiency of DHX9 possibly participates in exacerbations of viral infection such as influenza in chickens.

Vitellogenin synthesis in the ovary of scallop, Patinopecten yessoensis: Control by estradiol-17 beta and the central nervous system.

Elucidation of a profile of scallop vitellin formation associated with oogenesis and its endocrine control, and identification of a vitellogenin synthesizing site were immunologically undertaken by using anti-scallop Vn serum. Vn content increased during ovarian growth and accounted for more than 80% of the water soluble protein of the ovary at the mature stage. In vivo injection of estradiol-17 beta (E(2)) resulted in an increase in Vn content in the ovary. In vitro accumulation of Vn in the ovarian tissue was promoted with E2 and a vitellogenesis promoting factor (VPF) from cerebral plus pedal ganglion which was heat stable, less than MW 10,000 and trypsin/chymotrypsin resistant. Estrogen receptor (ER)-like immunoreactivity was found in the growing oocyte and the auxiliary cell in close contact with growing oocytes, in which Vn immunoreactivity was also found. It is suggested that the vitellogenin synthesis occurred inside the ovary, especially in the auxiliary cell, and is controlled by E2 and VPF via ER.