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Une étude récente par une équipe de chercheurs Chinois a démontré que la vaccination par le vaccin de l'hépatite B serait comme une cause de l'autisme en bloquant la neurogenèse des nouveaux nes. On trouve chez enfants vaccines par la vaccine de HBV beaucoup de marqueurs d'une inflammation chronique comme une elevation dans l'Il6, un marqueur connu dans plusieurs pathologies psychiatriques ( ADHD, autism) et une réponse th2 disproportionnée
source: https://www.ncbi.nlm.nih.gov/pubmed/27501128
Neonatal hepatitis B vaccination impaired the behavior and
neurogenesis of mice transiently in early adulthood
Junhua Yanga,1, Fangfang Qi a,1, Yang Yanga, Qunfang Yuana, Juntao Zoua, Kaihua Guoa,
Zhibin Yaoa,b,∗
a Department of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat-sen University, PR China b Guangdong Province Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat-sen University, PR China
a r t i c l e i n f o
Article history:
Received 21 February 2016
Received in revised form 9 July 2016
Accepted 1 August 2016
Keywords:
T helper bias
Cytokine
Microglia
Brain
Cognition
a b s t r a c t
The immune system plays a vital role in brain development. The hepatitis B vaccine (HBV)is administered
to more than 70% of neonates worldwide. Whether this neonatal vaccination affects brain development
is unknown. Newborn C57BL/6 mice were injected intraperitoneally with HBV or phosphate-buffered
saline. HBV induced impaired behavioral performances and hippocampal long-term potentiation at
8 weeks (w) of age without influence at 4 or 12 w. At 6 w, there was decreased neurogenesis, M1
microglial activation and a neurotoxic profile of neuroimmune molecule expression [increased tumor
necrosis factor- and reduced interferon (IFN)-, brain-derived neurotrophic factor and insulin-like
growth factor-1]in the hippocampus ofthe HBV-vaccinated mice. In the serum, HBVinduced significantly
higher levels of interleukin (IL)-4, indicating a T helper (Th)-2 bias. Moreover, the serum IFN-/IL-4 ratio
was positively correlated with the levels of neurotrophins and neurogenesis in the hippocampus at the
individual level. These findings suggest that neonatal HBV vaccination of mice results in neurobehavioral
impairments in early adulthood by inducing a proinflammatory and low neurotrophic milieu in the
hippocampus, which follows the HBV-induced systemic Th2 bias.
© 2016 Elsevier Ltd. All r
neurogenesis of mice transiently in early adulthood
Junhua Yanga,1, Fangfang Qi a,1, Yang Yanga, Qunfang Yuana, Juntao Zoua, Kaihua Guoa,
Zhibin Yaoa,b,∗
a Department of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat-sen University, PR China b Guangdong Province Key Laboratory of Brain Function and Disease, Zhongshan School of Medicine, Sun Yat-sen University, PR China
a r t i c l e i n f o
Article history:
Received 21 February 2016
Received in revised form 9 July 2016
Accepted 1 August 2016
Keywords:
T helper bias
Cytokine
Microglia
Brain
Cognition
a b s t r a c t
The immune system plays a vital role in brain development. The hepatitis B vaccine (HBV)is administered
to more than 70% of neonates worldwide. Whether this neonatal vaccination affects brain development
is unknown. Newborn C57BL/6 mice were injected intraperitoneally with HBV or phosphate-buffered
saline. HBV induced impaired behavioral performances and hippocampal long-term potentiation at
8 weeks (w) of age without influence at 4 or 12 w. At 6 w, there was decreased neurogenesis, M1
microglial activation and a neurotoxic profile of neuroimmune molecule expression [increased tumor
necrosis factor- and reduced interferon (IFN)-, brain-derived neurotrophic factor and insulin-like
growth factor-1]in the hippocampus ofthe HBV-vaccinated mice. In the serum, HBVinduced significantly
higher levels of interleukin (IL)-4, indicating a T helper (Th)-2 bias. Moreover, the serum IFN-/IL-4 ratio
was positively correlated with the levels of neurotrophins and neurogenesis in the hippocampus at the
individual level. These findings suggest that neonatal HBV vaccination of mice results in neurobehavioral
impairments in early adulthood by inducing a proinflammatory and low neurotrophic milieu in the
hippocampus, which follows the HBV-induced systemic Th2 bias.
© 2016 Elsevier Ltd. All r