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Dietary Postbiotics Reduce Cytotoxicity and Inflammation Induced by Crystalline Silica in an In Vitro RAW 264.7 Macrophage Model

Crystalline silica (cSiO(2)) particles are naturally existing environmental toxicants. Exposure to cSiO(2) could cause local or systemic inflammation and aggregate inflammation-associated diseases. Dietary postbiotics are reported to possess anti-inflammatory activities; however, their effects on cS...

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Detalles Bibliográficos
Autores principales: Du, Xue, Rodriguez, Jessica, Wee, Josephine
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8955347/
https://www.ncbi.nlm.nih.gov/pubmed/35327299
http://dx.doi.org/10.3390/foods11060877
Descripción
Sumario:Crystalline silica (cSiO(2)) particles are naturally existing environmental toxicants. Exposure to cSiO(2) could cause local or systemic inflammation and aggregate inflammation-associated diseases. Dietary postbiotics are reported to possess anti-inflammatory activities; however, their effects on cSiO(2)-triggered inflammation are unknown. Here, we investigate the impact of postbiotics from Lacticaseibacillus rhamnosus (LGG), Limosilactobacillus reuteri (L.reu), and Bifidobacterium animalis subsp. lactis Bb12 (BB12) on cSiO(2)-induced cytotoxicity and IL-1 cytokines in vitro using macrophages. The postbiotics used in this study were cell-free fractions of a probiotic growth medium collected at different time points. The in vitro model used was the wild-type murine macrophage RAW 264.7 cell line stably transfected with the inflammasome adapter protein, ASC. Our results indicate that all the postbiotics could reduce cSiO(2)-induced cytotoxicity in the wild-type and ASC macrophages and the effects were OD-dependent. Following priming with a lipopolysaccharide, cSiO(2) treatment resulted in robust inflammasome activation in ASC, as reflected by the IL-1β release. These responses were minimal or absent in the wild-type RAW cells. All the postbiotics decreased the release of IL-1β from ASC; however, only LGG and BB12 reduced the IL-1β secretion from wild-type cells. Only the L.reu postbiotics reduced the IL-1α release from ASC. We conclude that the postbiotics from LGG, BB12, and L.reu can protect macrophages against cSiO(2)-induced cytotoxicity and suppress IL-1β activation.