Papel dos receptores beta 2-adrenérgicos na resposta inflamatória a listeria monocytogenes em modelo murino.

Detalhes bibliográficos
Ano de defesa: 2024
Autor(a) principal: Gabriel Henrique Guimarães
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de Minas Gerais
Brasil
VETER - ESCOLA DE VETERINARIA
Programa de Pós-Graduação em Ciência Animal
UFMG
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: http://hdl.handle.net/1843/77851
Resumo: The sympathetic nervous system, mediated by catecholamines through adrenergic receptors (ARs), plays a role in the immune response, predominantly immunosuppressive. This study focuses on beta-adrenergic receptors (βARs), specifically the β2AR subtype, and its role in immune responses in a murine model of Listeria monocytogenes infection, an important foodborne zoonotic pathogen that causes clinical conditions such as abortions, meningoencephalitis, and septicemic infections. C57/BL6 WT, β2AR-/- mice and mice treated with βAR antagonists (nadolol and ICI 118,551) evaluated in acute infection by L. monocytogenes. Analyses of bacterial recovery, histopathological evaluation, immunohistochemistry, and cytokine measurement were performed. The absence of β2AR and pharmacological blockade significantly reduced bacterial recovery. Serum levels of IFN-γ increased, but there was no significant change in the IL-10 profile. β2AR-/- mice showed a lower histopathological lesion score, while βAR antagonists did not reduce the degree of tissue damage. The reduction in bacterial recovery, increased IFN-γ, and less severe histopathological lesions in β2AR-/- mice indicate a more effective response against the pathogen. However, pharmacological blockade reproduced partially this effect, possibly due to drug pharmacokinetics.