Bi-directional elucidation of Lactiplantibacillus plantarum (RTA 8) intervention on the pathophysiology of gut-brain axis during Salmonella brain infection

Abstract

Background There have been reports of patients suffering from typhoid fever, particularly those involving infants and immunocompromised patients, which at times present with Salmonella induced brain infection. Although rare, it has frequently been associated with adverse neurological complications and increased mortality. In this context, the gut-brain axis, involving two-way communication between the gut and the brain, holds immense significance as various gut ailments have been associated with psychiatric complications. In turn, several neurodegenerative diseases have been associated with an altered gut microbiota profile. Given the paucity of effective antimicrobials and increasing incidence of multi-drug resistance in pathogens, alternate treatment therapies such as probiotics have gained significant attention in the recent past. Results In the current study, prophylactic effect of Lactiplantibacillus plantarum (RTA 8) in preventing neurological complications occurring due to Salmonella brain infection was evaluated in a murine model. Along with a significant reduction in bacterial burden and improved histoarchitecture, L. plantarum (RTA 8) administration resulted in amelioration in the level of neurotransmitters such as serotonin, norepinephrine and dopamine in the gut as well as in the brain tissue. Simultaneously, increased gene expression of physiologically essential molecules such as mucin (MUC1 and MUC3) and brain-derived neurotrophic factor (BDNF) was also observed in this group. Conclusion Present study highlights the potential benefits of a probiotic supplemented diet in improving various aspects of host health due to their multi-targeted approach, thereby resulting in multi-faceted gains.

Comprehensive Review on Potential Signaling Pathways Involving the Transfer of α-Synuclein from the Gut to the Brain That Leads to Parkinson’s Disease

“…Toxins produced by microbes in the gut have been proposed to play a key role in the pathogenesis of PD by inducing the production of α-syn aggregates in the ENS, which then spread in a prion-like fashion through the vagus nerve to the CNS. Systemic inflammation could be encouraged by an overactive innate immune system caused by intestine bacterial overgrowth or gut dysbiosis, and the activation of enteric glial cells and enteric neurons could contribute to α-synucleinopathy. , The signaling molecules neuropeptide Y (NpY), cholecytokinin (CCK), ghrelin, and leptin, as well as neurotransmitters and glutamate, are thought to be the primary means of communication through GABA. , Neurotransmitter levels are reduced in PD . Microbiome-derived metabolites, or microbial metabolites, are small molecules that have been shown to affect host neurophysiology in various ways.…”

“…56,57 Neurotransmitter levels are reduced in PD. 58 Microbiome-derived metabolites, or microbial metabolites, are small molecules that have been shown to affect host neurophysiology in various ways. These include the circulatory system, the humoral system, the immune system, and the neuronal system.…”

Fecal microbiota transplantation in treating methylmercury-poisoned rats: Reconstruction of gut microbiome and modulation of gut-brain axis related metabolites

“…It indicated that MeHg disturbed the secretion of BDNF in the intestine and brain due to the damage to intestinal and brain structures.These results indicated that fecal transplantation could regulate BDNF and treat MeHg neurotoxicity. 50% of dopamine in the human body is secreted by the gut, so the decrease of dopamine secretion in the gut directly affects the whole body's dopamine metabolism [53] . The discovery that MeHg can induce the secretion of dopamine in the gut, brain and serum proves that MeHg does affect the gut brain axis system, and fecal transplantation can indeed repair such changes.…”