Abstract The gut microbiota is increasingly recognized as a systemic regulator of host physiology, extending its influence to the skin. Microbial metabolites—including short-chain fatty acids, exopolysaccharides, β-glucuronidase, and S-equol—modulate key processes such as inflammation, estrogen metabolism, and cellular senescence. In melasma, a chronic hyperpigmentation disorder with inflammatory features, dysbiosis alters immunometabolic pathways that sustain disease persistence. Beneficial taxa such as Faecalibacterium prausnitzii, Bacteroides thetaiotaomicron, Lactobacillus, and Bifidobacterium generate bioactive products that inhibit NF-κB signalling, suppress the senescence-associated secretory phenotype, and mitigate melanogenic stimuli. Conversely, β-glucuronidase-producing microbes enhance estrogen recycling and oxidative stress, favouring hyperpigmentation. This mini-review highlights microbial drivers of gut–skin crosstalk in melasma and underscores the microbiota as a source of potential biomarkers and therapeutic targets. We propose that gut dysbiosis contributes to melasma pathogenesis through microbiota-derived metabolites that modulate estrogen signalling and cellular senescence pathways, establishing a mechanistic framework linking immunometabolic dysregulation to persistent hyperpigmentation.
Cornachini et al. (Tue,) studied this question.