Apoptosis induction in duck tissues during duck hepatitis A virus type 1 infection.

To investigate the role of apoptosis in duck viral hepatitis pathogenesis, 4- and 21-d-old ducks were inoculated with duck hepatitis A virus serotype 1 and killed at 2, 6, 12, 24, and 48 h postinfection. TdT-mediated dUTP nick-end labeling was used to detect apoptosis cells. Expression profiles of apoptosis-related genes including caspase-3, -8, -9, and Bcl-2 in spleen, bursa of Fabricius, liver, and the quantity of virus in blood were examined using real-time PCR. The TdT-mediated dUTP nick-end labeling analysis indicated there was a significant difference of apoptotic cells between treatments and controls. The same difference also appeared in virus amount variation in blood during infection. Gene expression analysis revealed that the apoptosis-related gene expression profile was different in the 2 groups, and also different between various organs. This study suggested that apoptosis may play an important role in duck hepatitis A virus serotype 1 infection, and apoptosis suppression might facilitate virus multiplication, resulting in the highest virus concentration in the host.

Cytokine gene expression in the livers of ducklings infected with duck hepatitis virus-1 JX strain.

Duck hepatitis virus type 1 (DHV-1) causes a highly contagious disease in ducklings and is often associated with liver necrosis, hemorrhages, and high mortality. In the current study, the expression levels of gene transcripts encoding proinflammatory cytokines and the virus were measured by quantitative reverse-transcription PCR in duck livers after infection with a DHV-1 JX isolate obtained from natural cases in Hubei Province, China. In addition, sera IL-1ß, IL-6, and alanine aminotransferase levels were quantified. Liver histopathology was examined following DHV-1 infection. The ducklings died within 1 to 2 d postinfection (d.p.i.) because of typical liver degeneration, hemorrhage, necrosis, and bile-duct epithelial cell proliferation. Transcripts of the cytokines IFN-α, IL-6, TNF-α, and IL-10 decreased by 0.5 d.p.i. and then gradually increased at 1 d.p.i. Similarly, DHV-1 JX 3D gene levels in the liver sharply increased at 1 d.p.i. and then maintained a high level. In contrast, liver TNF-α and IL-1ß transcripts showed no increased expression of the cytokine gene postinfection and significantly decreased compared with the expression at 0.25 d.p.i., only the expression of IFN-α transcripts increased 128-fold by 1 d.p.i. Changes in the serum IL-6 level remained relatively stable postinfection and not significantly different compared with that of the control (P > 0.05), whereas serum levels of IL-1ß significantly decreased at 0.5 d.p.i. and increased from 1 d.p.i. onwards (P < 0.05). Serum alanine aminotransferase levels significantly increased 2 d.p.i. compared with that of the control group (P < 0.01), which seemed to keep with the number of dead ducks. The cytokines exhibited a biphasic pattern following DHV-1 JX infection. Taken together, the data indicated that duckling liver inflammatory responses were produced following experimental DHV-1 JX infection involving multiple cytokines.

Role of interleukin-6 in the pathogenesis of an avian model of Staphylococcus aureus arthritis.

To evaluate the role of interleukin-6 (IL-6) in arthritis induced by Staphylococcus aureus, a chicken model was developed for study. A total of 120 healthy broilers (8 wk old) were randomly divided into 4 groups. Two groups were injected with 0.35 mL of Staph. aureus (7.1x10(9) cfu/mL) into the right hock joints and the other 2 were injected with 0.35 mL of sterile saline into the same joints. One group of each of the 2 treatment groups was fed levofloxacin at a dose of 5 mg/kg of BW on the third day postinoculation for 4 successive days. Chicken blood samples were obtained on d 0, 1, 4, 7, 14, 21, 28, and 35 postinoculation. Chicken IL-6 (chIL-6) activities and concentrations in serum were quantified by B9 bioassay and human IL-6 ELISA, respectively. The results showed that chIL-6 activities and concentrations were reduced (P<0.05) in the serum of infected broilers treated with levofloxacin compared with birds injected only with Staph. aureus. Levofloxacin treatment had no effect on IL-6 activities and concentrations in uninfected broilers. There was a strong correlation (r=0.91) between serum chIL-6 activities by the B9 bioassay and serum IL-6 concentrations determined by the human IL-6 ELISA. We concluded that chIL-6 is involved in the progression of chicken arthritis induced by Staph. aureus, and that it contributes to disease incidence and mortality.