Understanding the relationship between microorganisms that live in our intestines and neuroinflammatory and neurodegenerative pathologies of the central nervous system (CNS) is essential, since they have been shown to have an immunomodulatory effect in neurological disorders, such as multiple sclerosis (MS). The gut microbiota can be affected by several environmental factors, including infections, physical and emotional stress and diet, the latter known as the main modulator of intestinal bacteria. An abrupt shift in the gut microbiota composition and function is known as dysbiosis, a state of local and systemic inflammation produced by pathogenic bacteria and its metabolites responsible for numerous neurological symptoms. It may also trigger neuronal damage in patients diagnosed with MS. Intestinal dysbiosis affects the permeability of the intestine, allowing chronic low-grade bacterial translocation from the intestine to the circulation, which may overstimulate immune cells and cells resident in the CNS, break immune tolerance and, in addition, alter the permeability of the blood-brain barrier (BBB). This way, toxins, inflammatory molecules and oxidative stress molecules can pass freely into the CNS and cause extensive damage to the brain. However, commensal bacteria, such as the Lactobacillus genus and Bacteroides fragilis, and their metabolites (with anti-inflammatory potential), produce neurotransmitters such as γ-aminobutyric acid, histamine, dopamine, norepinephrine, acetylcholine and serotonin, which are important for neurological regulation. In addition, reprogramming the gut microbiota of patients with MS with a healthy gut microbiota may help improve the integrity of the gut and BBB, by providing clinically protective anti-inflammatory effects and reducing the disease's degenerative progression. The present review provides valuable information about the relationship between gut microbiota and neuroinflammatory processes of the CNS. Most importantly, it highlights the importance of intestinal bacteria as an environmental factor that may mediate the clinical course of MS, or even predispose to the outbreak of this disease.