Gallic acid promotes macrophage phagosome acidification and phagolysosome formation by activating NLRP3/mTOR signaling pathway.
J Infect Chemother
; 30(9): 867-875, 2024 Sep.
Article
en En
| MEDLINE
| ID: mdl-38462174
ABSTRACT
INTRODUCTION:
Gallic acid (GA) has a good therapeutic effect in bacteriological inhibition and plays a variety of functions in maintaining the stability of the immune system. The aim of the present study was to investigate the effect of GA on the bactericidal activity of macrophages against Vibrio vulnificus (Vv).METHODS:
A cell counting kit-8 (CCK-8) assay was carried out to test the cytotoxicity of GA on J774A.1 cells. Concentration of proinflammatory cytokines in J774A.1 cells were evaluated by ELISA. The internalization and degradation of Vv in the phagosomes were observed by transmission electron microscopy (TEM). The phagosome acidification and phagolysosome formation were detected to evaluate the bacteria-clearing function of J774A.1 cells. The bactericidal activity of GA in vivo was also investigated by collecting the survival time of Vv infected mice and observing the inflammatory infiltration of organs.RESULTS:
Our results demonstrated that GA at 50 µM significantly inhibited the proinflammatory cytokines levels, promoted phagosome acidification and phagolysosome formation in J774A.1 cells with Vv infection. This may be related to the activation of NLRP3/mTOR signaling pathway. Additionally, GA treatment improves the survival and bactericidal activity of mice infected with Vv.CONCLUSIONS:
In summary, GA exerts bactericidal activity against Vv infection by regulating the formation and acidification of phagocytic lysosomes in macrophages.Palabras clave
Texto completo:
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Base de datos:
MEDLINE
Asunto principal:
Fagosomas
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Transducción de Señal
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Vibrio vulnificus
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Serina-Treonina Quinasas TOR
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Proteína con Dominio Pirina 3 de la Familia NLR
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Ácido Gálico
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Macrófagos
Idioma:
En
Revista:
J Infect Chemother
Asunto de la revista:
MICROBIOLOGIA
/
TERAPIA POR MEDICAMENTOS
Año:
2024
Tipo del documento:
Article