Effects of interleukin (IL)-1β and tumor necrosis factor (TNF)-α on betanodavirus-induced neuron death
Date Issued
2016
Date
2016
Author(s)
Chiang, Yu-Hui
Abstract
Nervous necrosis virus (NNV), a non-enveloped virion with two single-stranded positive-sense RNAs, belongs to betanodavirus genus of Nodaviridae family. NNV is the causative agent of viral nervous necrosis (VNN) disease, which has caused mass mortality and economic loss in many species of cultured marine fish, including groupers (Epinephelus spp.). The pathological characteristic of VNN is the vacuolization and necrosis of brain and retina. Our team has found that the expression level of interleukin (IL)-1β gene became very high in the brain of moribund groupers with VNN. Whether IL-1β cytokine played a critical role in the neuronal death of NNV-infected groupers is unclear, and is clarified in this study. The primary tissue culture of grouper brain (pGB cells) was established, and was infected with NNV. NNV infection caused the proliferation of microglia and death of neurons in pGB cells, and the amount of dead neurons was viral load-dependent. Viral capsid protein was detected in the neuron and microglia, but not in the astrocytes. The microglia in pGB cells released IL-1β and tumor necrosis factor (TNF)-α in the CS at 3 days post infection (dpi). NNV-specific polyclonal antibodies were used to neutralize NNV. The CS collected at 3 dpi, treated with or without NNV-specific polyclonal antibodies, was separately added into two sets of new pGB cells, and both were able to induce neuronal death in pGB cells. Also, the neurotoxic effect in CS-treated pGB cells was attenuated by pre-adding anti-IL-1β pAb in the CS. Moreover, treatment of pGB cells with combination of NNV and rIL-1β resulted in more dead neurons, compared to sole infection of NNV. We therefore suggested that the IL-1β secreted by NNV-infected pGB cells play an important role for the induction of neuronal death and IL-1β in CS was the substance for neurotoxic effect that caused more serious neuronal death after NNV infection.
Subjects
Interleukin (IL)-1β
neuroinflammation
betanodavirus
grouper
microglia
SDGs
Type
thesis
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