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Galantamine attenuates autoinflammation in a mouse model of familial mediterranean fever

BACKGROUND: Autoinflammatory diseases, a diverse group of inherited conditions characterized by excessive innate immune activation, have limited therapeutic options. Neuroimmune circuits of the inflammatory reflex control innate immune overactivation and can be stimulated to treat disease using the...

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Detalles Bibliográficos
Autores principales: Mughrabi, Ibrahim T., Ochani, Mahendar, Tanovic, Mirza, Wang, Ping, Diamond, Betty, Sherry, Barbara, Pavlov, Valentin A., Ozen, Seza, Kastner, Daniel L., Chae, Jae Jin, Al-Abed, Yousef
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9733251/
https://www.ncbi.nlm.nih.gov/pubmed/36494621
http://dx.doi.org/10.1186/s10020-022-00571-9
Descripción
Sumario:BACKGROUND: Autoinflammatory diseases, a diverse group of inherited conditions characterized by excessive innate immune activation, have limited therapeutic options. Neuroimmune circuits of the inflammatory reflex control innate immune overactivation and can be stimulated to treat disease using the acetylcholinesterase inhibitor galantamine. METHODS: We tested the efficacy of galantamine in a rodent model of the prototypical autoinflammatory disease familial Mediterranean fever (FMF). Multiple chronic disease markers were evaluated in animals that received long-term galantamine treatment compared to vehicle. RESULTS: Long-term treatment with galantamine attenuated the associated splenomegaly and anemia which are characteristic features of this disease. Further, treatment reduced inflammatory cell infiltration into affected organs and a subcutaneous air pouch. CONCLUSIONS: These findings suggest that galantamine attenuates chronic inflammation in this mouse model of FMF. Further research is warranted to explore the therapeutic potential of galantamine in FMF and other autoinflammatory diseases. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s10020-022-00571-9.