6533b7ddfe1ef96bd12736a6
RESEARCH PRODUCT
Role of Microbiota-Derived Extracellular Vesicles in Gut-Brain Communication
María PascualJuan UreñaConsuelo GuerriCarlos M. Cuestasubject
0301 basic medicineLipopolysaccharideQH301-705.5brainReviewBiologymedicine.disease_causeCatalysisInorganic ChemistryNeuroblastoma03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemmedicinemicrobiotaAnimalsHumansPhysical and Theoretical ChemistryBiology (General)ReceptorbacteriaMolecular BiologyQD1-999SpectroscopyGastrointestinal tractneuropathologyOrganic ChemistryPathogenic bacteriaGeneral Medicinemedicine.diseaseIntestinal epitheliumComputer Science ApplicationsCell biologyChemistry030104 developmental biologychemistryRNA Long Noncodingextracellular vesiclesDysbiosis030217 neurology & neurosurgeryHomeostasisdescription
Human intestinal microbiota comprise of a dynamic population of bacterial species and other microorganisms with the capacity to interact with the rest of the organism and strongly influence the host during homeostasis and disease. Commensal and pathogenic bacteria coexist in homeostasis with the intestinal epithelium and the gastrointestinal tract’s immune system, or GALT (gut-associated lymphoid tissue), of the host. However, a disruption to this homeostasis or dysbiosis by different factors (e.g., stress, diet, use of antibiotics, age, inflammatory processes) can cause brain dysfunction given the communication between the gut and brain. Recently, extracellular vesicles (EVs) derived from bacteria have emerged as possible carriers in gut-brain communication through the interaction of their vesicle components with immune receptors, which lead to neuroinflammatory immune response activation. This review discusses the critical role of bacterial EVs from the gut in the neuropathology of brain dysfunctions by modulating the immune response. These vesicles, which contain harmful bacterial EV contents such as lipopolysaccharide (LPS), peptidoglycans, toxins and nucleic acids, are capable of crossing tissue barriers including the blood-brain barrier and interacting with the immune receptors of glial cells (e.g., Toll-like receptors) to lead to the production of cytokines and inflammatory mediators, which can cause brain impairment and behavioral dysfunctions.
year | journal | country | edition | language |
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2021-04-01 | International Journal of Molecular Sciences |