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https://www.arca.fiocruz.br/handle/icict/51284
BRAIN-DERIVED NEUROTROPHIC FACTOR IS DOWN REGULATED AFTER BOVINE ALPHA-HERPESVIRUS 5 INFECTION IN BOTH WILD-TYPE AND TLR3/7/9 DEFICIENT MICE
Author
Silva, Daniele Gonçalves da
Carvalho, Iracema Luisa Quintino de
Toscano, Eliana Cristina de Brito
Santos, Beatriz Álvares da Silva Senra
Oliveira, Bruna da Silva
Campos, Marco Antônio
Fonseca, Flávio Guimarães da
Camargos, Quezya Mendes
Sousa, Gabriela Ferreira de
Caliari, Marcelo Vidigal
Teixeira, Antônio Lúcio
Miranda, Aline Silva de
Alvarenga, Milene
Carvalho, Iracema Luisa Quintino de
Toscano, Eliana Cristina de Brito
Santos, Beatriz Álvares da Silva Senra
Oliveira, Bruna da Silva
Campos, Marco Antônio
Fonseca, Flávio Guimarães da
Camargos, Quezya Mendes
Sousa, Gabriela Ferreira de
Caliari, Marcelo Vidigal
Teixeira, Antônio Lúcio
Miranda, Aline Silva de
Alvarenga, Milene
Affilliation
Laboratory of Cellular and Molecular Pathology. Department of General Pathology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Microbiology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Laboratory of Cellular and Molecular Pathology. Department of General Pathology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Laboratory of Animal Virology. Department of Preventive Veterinary Medicine. Veterinary School. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Morphology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
René Rachou Institute. Oswaldo Cruz Foundation. Belo Horizonte, MG, Brazil.
Department of Microbiology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Laboratory of Cellular and Molecular Pathology. Department of General Pathology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Laboratory of Cellular and Molecular Pathology. Department of General Pathology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Laboratory of Cellular and Molecular Pathology. Department of General Pathology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Neuropsychiatry Program. Department of Psychiatry and Behavioral Sciences. School of Medicine. University of Texas Health Science. Houston, TX, USA.
Department of Morphology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Laboratory of Cellular and Molecular Pathology. Department of General Pathology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Microbiology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Laboratory of Cellular and Molecular Pathology. Department of General Pathology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Laboratory of Animal Virology. Department of Preventive Veterinary Medicine. Veterinary School. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Morphology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
René Rachou Institute. Oswaldo Cruz Foundation. Belo Horizonte, MG, Brazil.
Department of Microbiology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Laboratory of Cellular and Molecular Pathology. Department of General Pathology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Laboratory of Cellular and Molecular Pathology. Department of General Pathology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Laboratory of Cellular and Molecular Pathology. Department of General Pathology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Neuropsychiatry Program. Department of Psychiatry and Behavioral Sciences. School of Medicine. University of Texas Health Science. Houston, TX, USA.
Department of Morphology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Laboratory of Cellular and Molecular Pathology. Department of General Pathology. Biological Science Institute. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Abstract
Neurotrophic factors have been implicated in the control of neuronal survival and plasticity in different brain diseases. Meningoencephalitis caused by bovine alpha-herpesvirus 5 (BoHV-5) infection is a frequent neurological disease of young cattle, being the involvement of apoptosis in the development of neuropathological changes frequently discussed in the literature. It's well known that Toll-like receptors (TLRs) can activate neuroinflammatory response and consequently lead to neuronal loss. However, there are no studies evaluating the expression of neurotrophic factors and their association with brain pathology and TLRs during the infection by BoHV-5. The current study aimed to analyze brain levels of neurotrophic factors along with neuropathological changes during acute infection by BoHV-5 in wild-type (WT) and TLR3/7/9 (TLR3/7/9-/-) deficiency mice. The infection was induced by intracranial inoculation of 1 × 104 TCID50 of BoHV-5. Infected animals presented similar degrees of clinical signs and neuropathological changes. Both infected groups had meningoencephalitis and neuronal damage in CA regions from hippocampus. BoHV-5 infection promoted the proliferation of Iba-1 positive cells throughout the neuropil, mainly located in the frontal cortex. Moreover, significant lower levels of brain-derived neurotrophic factor (BDNF) were detected in both BoHV-5 infected WT and TLR3/7/9 deficient mice, compared with non-infected animals. Our study showed that BDNF down regulation was associated with brain inflammation, reactive microgliosis and neuronal loss after bovine alpha-herpesvirus 5 infection in mice. Moreover, we demonstrated that combined TLR3/7/9 deficiency does not alter those parameters.
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