Camel milk-based probiotics: functional properties, gut health benefits, and emerging implications for the gut-brain...

Camel milk is gaining scientific interest for its unique composition, including bioactive proteins, high antimicrobial peptides (lactoferrin, lysozyme), immunomodulatory components, and lower allergenic potential compared to bovine milk, positioning it as a promising matrix for probiotic delivery. Probiotics support gut homeostasis and may influence the gut-brain axis via microbial metabolites (SCFAs, GABA), immune modulation, and neuroactive compound production. This review critically assesses current evidence on camel milk-based probiotics, emphasizing functional properties, effects on gut microbiota, gastrointestinal benefits, and emerging implications for the gut-brain axis (inflammation reduction, metabolic signaling, neurotransmitter pathways). Drawing from in vitro studies, animal models (e.g., colitis, EAE, diabetes), and limited human trials, we evaluate translational relevance. Preliminary findings suggest benefits in gut health, microbiota modulation, and potential neuroprotection, but strain specificity, mechanistic details, and robust clinical efficacy remain limited. Significant knowledge gaps persist regarding optimal strains, dosing, and long-term effects. Rigorous, well-designed preclinical and clinical studies are essential to validate health claims and support development of camel milk-based functional products targeting gut and potential neurological health.

The graphical abstract illustrates camel milk-derived probiotics as modulators of the gut-brain axis through interconnected pathways. Central mechanisms include microbiota modulation, synthesis of neuroactive compounds (SCFAs, GABA, neurotransmitters), immune regulation, and anti-inflammatory effects. Bidirectional communication between gut and brain occurs via neural, endocrine, and metabolic routes, with potential therapeutic applications for mental health disorders including depression, anxiety, and cognitive impairment.

The online version contains supplementary material available at 10.1007/s13197-026-06765-x.