Immunocompetence of the 2001 Ross 308 broiler strain and the 1957 Athens Canadian Randombred Control (ACRBC) strain was compared when they were given diets representative of those that were being used in 1957 and 2001. Antibody response against SRBC, in vivo lymphoproliferation against Phytohemagglutinin-P (PHA-P), and inflammatory and phagocytic responses of the macrophages were measured. The Ross 308 strain on the 2001 diet had higher BW at 24 d of age (P = 0.0001), whereas the ACRBC had greater lymphoid organ weights (except thymus) relative to BW (P < or = 0.003). The ACRBC strain showed greater antibody responses against SRBC than the 2001 Ross 308 birds for much of the trial (P < or = 0.0362). However, the Ross 308 broilers had greater PHA-P-induced toe-web swelling response (P < or = 0.0129). Inflammatory exudate cell numbers were higher in the Ross 308 broilers than in the ACRBC birds (P = 0.0261). The percentage of macrophages that phagocytized SRBC was comparable between the two strains, but the number of SRBC phagocytized by individual macrophages was higher (P = 0.0122) in the Ross 308 broiler than in the ACRBC chickens. Nitrite production by macrophages following lipopolysacharide stimulation was comparable between the two strains. Interactions of diet, strain, and sex were inconsistent among all parameters tested. In conclusion, the current study suggested that genetic selection for improved broiler performance has resulted in a decrease in the adaptive arm of the immune response but an increase in the cell-mediated and inflammatory responses.
The immunological performance of modern turkeys (one-third each of the Nicholas Turkey, British United Turkeys of America, and Hybrid Turkey strains) hatched in 2003 (2003 strain) was compared with that of a randombred control turkey strain (RBC2) established in calendar year 1966, when fed representative 1966 and 2003 type diets. The 2003 strain had a higher BW and bursa of Fabricius weight relative to total BW compared with the RBC2 strain (P = 0.0001) when measured at 12 and 13 d of age, respectively. Total antibody response against SRBC did not differ between strains, nor were any differences observed in the IgM antibody levels either during a primary or secondary SRBC challenge. However, RBC2 poults had higher IgG levels (P = 0.02) than the 2003 strain at 7 d post secondary SRBC challenge. No significant differences were observed in the phytohemagglutinin phosphate-mediated toe-web lymphoblastic response. However, the 2003-strain turkeys seemed to have a better swelling response (P = 0.06) than the RBC2-strain turkeys when measured at 24 h post phytohemagglutinin phosphate injection. The modern turkeys also had higher mononuclear phagocytic system function, as measured by clearance of carbon particles from the bloodstream 5 min post intravenous injection of colloidal carbon (P = 0.02). These results indicate that selection over the years of turkeys for improved performance traits has had no adverse effects on most of the immune system indicators when examined prior to sexual maturity in the current study.
An avian reovirus, ARV-CU98, has recently been isolated from poults experiencing poult enteritis and mortality syndrome (PEMS). To further understand ARV-CU98 and its role in PEMS, the current study investigates interactions of ARV-CU98 with various cell types in vitro. When macrophages, B cells, T cells, and liver cells of chicken or turkey origin were co-incubated with ARV-CU98, only cells of liver origin demonstrated cytopathic effects, the presence of viral antigen, and reduced metabolic activity over time. Furthermore, distinctive pockets of viral particles were evident in electron microscopic examination of a chicken hepatocellular carcinoma (LMH) cell line, but not in a chicken macrophage cell line (MQ-NCSU) co-incubated with virus. Additional evidence of viral replication in LMH, cells but not MQ-NCSU cells was demonstrated by the presence of two viral bands (43 and 145 kD size) in cell lysates from LMH cells exposed to ARV-CU98. Although not capable of being infected by ARV-CU98, MQ-NCSU cells do appear to be activated by the virus since IL-1 mRNA expression is increased in MQ-NCSU cells 2 h after addition of the virus. LMH cells exposed to the virus demonstrate a decrease in IL-1 mRNA expression by 8 to 10 h after addition of the virus, perhaps corresponding to the initiation of infection by the virus. In conclusion, this study demonstrates that ARV-CU98 actively infects and replicates in LMH cells, but not in lymphocytes or macrophages, suggesting that the liver may be a target and site of replication of ARV-CU98 in poults experiencing PEMS.
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