https://orcid.org/0000-0001-8999-5048
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ABSTRACT
A close communication exists between the microorganisms that live in the intestine and the brain, the so-called microbiota-gut-brain axis. This interaction occurs at different levels, such as the induction by bacteria of an inflammatory state in the intestine that produces (i) stimulation of the vagus nerve that conducts information to the brain, and (ii) the release of proinflammatory cytokines – such as TNF-α- to circulation, which can then be transported to the brain and trigger neuroinflammation. Ethanol-induced neuroinflammation is produced, in part, by the impairment of the epithelial barrier function of the intestine, since acetaldehyde generated in the gut from ethanol oxidation produces a disassembly of the tight junctions (TJ), which allows diffusion of bacterial components into the blood; these events trigger a systemic inflammatory response that crosses the blood-brain barrier and induce neuroinflammation. Some short-chain fatty acids (SCFAs) such as butyrate, propionate, and acetate, are produced from indigestible polysaccharides (fibers) by certain bacteria in the microbiota. These SCFAs have shown a protective function of the TJ against intestinal injuries, preserving the intestinal barrier function. In this perspective article, we discuss the therapeutic possibility to increase the production of SCFAs in the intestine of patients with AUD, to protect the integrity of TJ and thus modulate the neuroinflammatory process that helps to the establishment of chronic alcohol intake. In this way, a new therapeutic alternative is proposed here through a simple dietary intervention in the patient, increasing their fiber consumption.
Disclosure statement
No potential conflict of interest was reported by the author(s).