Skin bromhidrosis, commonly referred to as body odor, is caused by the microbial breakdown of sweat, leading to the formation of volatile organic compounds (VOCs) that result in unpleasant odors. While body odor is a natural consequence of sweat production, excessive or persistent odor can significantly affect quality of life, causing social stigma and psychological distress. Traditional approaches to managing body odor, such as antiperspirants and deodorants, have limitations, necessitating the development of more advanced diagnostic tools and treatments. This review aims to explore recent advancements in the diagnosis and treatment of skin offensive odor, focusing on cutting-edge technologies and novel approaches. It highlights the interplay of the skin microbiome, sweat gland activity, and external factors in odor formation and investigates innovative solutions for long-term odor management. Emerging diagnostic techniques, such as electronic nose (E-nose) technology, gas chromatography-mass spectrometry (GC-MS), and next-generation sequencing (NGS), enable precise detection and analysis of odor-causing VOCs and microbial profiles. These tools facilitate a deeper understanding of the pathophysiology of odor production. Treatment innovations include nanotechnology-based antimicrobials (e.g., silver and zinc oxide nanoparticles), probiotic formulations for microbiome modulation, and odor-neutralizing compounds such as cyclodextrins and enzymatic neutralizers. Advanced delivery systems, including microneedle patches and nanoencapsulation, enable targeted, sustained release of active ingredients. Additionally, systemic approaches like oral probiotics and dietary interventions offer complementary strategies for managing body odor. The integration of novel diagnostics with innovative topical and systemic treatments offers promising avenues for more effective and personalized management of skin offensive odor. These advancements pave the way for improved quality of life for individuals affected by bromhidrosis, with potential for widespread application in personal care and medical contexts. Clinical trial number: Not applicable.

Axillary osmidrosis (AO) affects a large number of young people in Asia, resulting from a combination of body and bacterial metabolism. This study aimed to explore the pathogenesis of AO through proteomics. Apocrine gland tissues from 3 mild and 3 severe AO patients were analyzed using 4D label-free proteomics, followed by bioinformatics analysis. The RNA and protein levels of the predicted key regulators were further validated by qPCR and immunohistochemistry in additional AO tissues. A total of 5066 proteins were identified, of which 323 were significantly upregulated and 412 were downregulated (by |log2FC|> 1 and p < 0.05). GO terms related to mitochondria, oxidation-reduction processes, and peroxisomes were significantly enriched among the upregulated DEPs, suggesting enhanced energy metabolism in severe AO patients. Downregulated DEPs were enriched in ribosome, phagosome, and platelet activation pathways according to KEGG, while upregulated DEPs were significantly enriched in metabolic pathways, valine, leucine, and isoleucine degradation, peroxisomes, and fatty acid degradation. The enriched pathways suggest that apocrine gland tissues develop AO by increasing blood flow to promote sweating and secreting excessive short-chain fatty acids by coupling mitochondrial respiration with incomplete metabolism of lipids and branched-chain amino acids. This metabolic coupling may have implications for studies on cardiovascular disease, metabolic disorders, and oxidative stress. Key proteins in the signaling network were further confirmed by qPCR and immunohistochemistry, including reduced FGA and ITGA2B, and increased EHHADH and ACOX1. Our proteomics analysis suggests a paradigm of lipid metabolism involving mitochondrial respiration and incomplete lipid and branched-chain amino acid metabolism as the pathogenesis of AO. We also suggest that EHHADH is a key regulator in promoting AO in this process.

The human armpit microbiome is metabolically entangled with skin cell physiology. This "meta-organism" symbiotic mutualism results in sweat either with or without odor (osmidrosis), depending on host ABCC11 gene haplotypes. Apocrine metabolism produces odorless S-glutathione conjugate that is transferred by ABCC11 transporters into secretory vesicles, deglutamylated to S-Cys-Gly-3M3SH thiol, and exuded to skin surface. An anthropogenic clade of skin bacteria then takes up the thiol and bioconverts it to malodorous 3-methyl-3-sulfanylhexan-1-ol (3M3SH). We hypothesized a familial meta-organism association of human ABCC11 gene non-synonymous SNP rs17822931 interplaying with skin microbiome 3M3SH biosynthesis. Subjects were genotyped for ABCC11 SNPs, and their haplotypes were correlated with axilla microbiome DNA sequencing profiles and predicted metagenome functions. A multigeneration family pedigree revealed a Mendelian autosomal recessive pattern: the C allele of ABCC11 correlated with bacterial Cys-S-conjugate β-lyase (PatB) gene known for Staphylococcus hominis biosynthesis of 3M3SH from human precursor; PatB was rescinded in hosts with homozygous TT alleles encoding ABCC11 loss-of-function mutation. We posit that a C allele encoding functional ABCC11 is key to delivering host conjugate precursors that shape heritable skin niche conditions favorable to harboring Staphylococcus having genomics of odor thiol production. This provides existential insights into human evolution and global regional population ancestries.

Inflammatory bowel disease (IBD) is a disorder of the immune system and intestinal microecosystem caused by environmental factors in genetically susceptible people. Paneth cells (PCs) play a central role in IBD pathogenesis, especially in Crohn's disease development, and their morphology, number and function are regulated by susceptibility genes. In the intestine, PCs participate in the formation of the stem cell microenvironment by secreting antibacterial particles and play a role in helping maintain the intestinal microecology and intestinal mucosal homeostasis. Moreover, PC proliferation and maturation depend on symbiotic flora in the intestine. This paper describes the interactions among susceptibility genes, PCs and intestinal microecology and their effects on IBD occurrence and development.

Corynebacterium accounts for around 20% of the armpit microbiome and plays an essential role in axillary osmidrosis (AO). In this study, the effects of Lactobacillus bulgaricus treatment on the microecological environment of armpits and its efficacy in the treatment of AO were investigated. A total of 10 AO patients were enrolled in this study. The patients were treated with L. bulgaricus mixed with saline on the left armpit (experimental group) and pure saline on the right armpit (control group) for 28 days. After treatment, AO severity showed a significant decrease (p = 0.013) in the experimental group compared with the control group, and the Corynebacterium abundance also showed a corresponding significant decrease (p < 0.01). Moreover, no significant variation in Staphylococcus abundance was found between these two groups. The microbe diversity is not disturbed in the treatment. Accordingly, our study demonstrates that L. bulgaricus can serve as an effective probiotic microbe for AO treatment by reducing the abundance of Corynebacterium and rebalancing the microecological environment.