The commensal bacterium Lactiplantibacillus plantarum imprints innate memory-like responses in mononuclear phagocytes
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Date
2021-07-05Author
Pellón Rodríguez, Aize
Barriales, Diego
Peña Cearra, Ainize
Castelo Careaga, Janire
Palacios, Ainhoa
López, Nerea
Atondo Gondra, Estibaliz
Pascual Itoiz, Miguel Ángel
Martín Ruiz, Itziar
Sampedro, Leticia
González López, Monika
Bárcena, Laura
Martín Mateos, Teresa
Landete, José María
Prados Rosales, Rafael
Plaza Vinuesa, Laura
Muñoz, Rosario
De las Rivas, Blanca
Rodríguez, Juan Miguel
Berra Ramírez, Miren Edurne
Aransay Bañares, Ana María
Lavín, José L.
Rodríguez López, Héctor
Anguita Castillo, Juan de Dios
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Gut Microbes 13(1) : (2021) // Article ID 1939598
Abstract
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.