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The commensal bacterium Lactiplantibacillus plantarum imprints innate memory-like responses in mononuclear phagocytes

Gut microbiota is a constant source of antigens and stimuli to which the resident immune system has developed tolerance. However, the mechanisms by which mononuclear phagocytes, specifically monocytes/macrophages, cope with these usually pro-inflammatory signals are poorly understood. Here, we show...

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Detalles Bibliográficos
Autores principales: Pellon, Aize, Barriales, Diego, Peña-Cearra, Ainize, Castelo-Careaga, Janire, Palacios, Ainhoa, Lopez, Nerea, Atondo, Estibaliz, Pascual-Itoiz, Miguel Angel, Martín-Ruiz, Itziar, Sampedro, Leticia, Gonzalez-Lopez, Monika, Bárcena, Laura, Martín-Mateos, Teresa, Landete, Jose María, Prados-Rosales, Rafael, Plaza-Vinuesa, Laura, Muñoz, Rosario, de las Rivas, Blanca, Rodríguez, Juan Miguel, Berra, Edurne, Aransay, Ana M., Abecia, Leticia, Lavín, Jose Luis, Rodríguez, Hector, Anguita, Juan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8259724/
https://www.ncbi.nlm.nih.gov/pubmed/34224309
http://dx.doi.org/10.1080/19490976.2021.1939598
Descripción
Sumario:Gut microbiota is a constant source of antigens and stimuli to which the resident immune system has developed tolerance. However, the mechanisms by which mononuclear phagocytes, specifically monocytes/macrophages, cope with these usually pro-inflammatory signals are poorly understood. Here, we show that innate immune memory promotes anti-inflammatory homeostasis, using as model strains of the commensal bacterium Lactiplantibacillus plantarum. Priming of monocytes/macrophages with bacteria, especially in its live form, enhances bacterial intracellular survival and decreases the release of pro-inflammatory signals to the environment, with lower production of TNF and higher levels of IL-10. Analysis of the transcriptomic landscape of these cells shows downregulation of pathways associated with the production of reactive oxygen species (ROS) and the release of cytokines, chemokines and antimicrobial peptides. Indeed, the induction of ROS prevents memory-induced bacterial survival. In addition, there is a dysregulation in gene expression of several metabolic pathways leading to decreased glycolytic and respiratory rates in memory cells. These data support commensal microbe-specific metabolic changes in innate immune memory cells that might contribute to homeostasis in the gut.