Huabing Zhao

Introduction: Atopic dermatitis (AD), a chronic inflammatory skin disorder, represents a significant global health challenge. Although probiotic therapy shows potential for skin disease management, the application of live bacteria remains associated with multiple limitations. Bacterial extracellular vesicles (EVs) may provide a safer and more effective alternative. Methods: In this study, EVs derived from Lactobacillus plantarum were isolated and characterized. Their therapeutic potential against AD was evaluated through in vitro and in vivo experiments. HaCaT keratinocytes were used to establish an AD-like cellular model, and an AD mouse model was induced using 2,4-dinitrofluorobenzene (DNFB). The effects of L. plantarum EVs on skin barrier function, inflammatory responses, and scratching behaviors were evaluated. Multi-omics analysis was performed to explore the potential bioactive components within EVs underlying their therapeutic effects. Results: In vitro , L. plantarum EVs were efficiently internalized by HaCaT keratinocytes, significantly increasing ceramide levels and upregulating key barrier-related genes, including filaggrin (FLG), desmoglein-1 (DSG1), and ceramide synthase 3 (CerS3), thereby enhancing skin barrier function in the AD-like cell model. Meanwhile, EVs treatment downregulated pro-inflammatory cytokines, including thymic stromal lymphopoietin (TSLP), interleukin-25 (IL-25), interleukin-33 (IL-33), and tumor necrosis factor-α (TNF-α). In the DNFB-induced AD mouse model, EVs administration markedly alleviated clinical symptoms, reduced lesion scores and transepidermal water loss, and restored epidermal thickness to near-normal levels, indicating barrier repair in AD mice. Skin tissue analysis further confirmed reduced inflammatory cytokine expression. Additionally, EVs suppressed scratching behaviors by inhibiting the IL-31 pathway. Multi-omics analysis suggested that the therapeutic effects of L. plantarum EVs may be associated with lipid-based bioactive components within EVs. Discussion: These findings indicate that bacterial EVs represent a promising probiotic-inspired strategy for AD treatment and provide new insights into the development of safe and effective dermatological therapies.

Acne vulgaris is a prevalent chronic inflammatory dermatosis primarily affecting the pilosebaceous units. Current therapeutic approaches often exhibit limited efficacy and high recurrence rates. To investigate the microbiome-related mechanisms of acne vulgaris, facial skin samples from 19 patients with moderate acne and 20 healthy individuals were analyzed using an integrated metagenomic and lipidomic profiling strategy. Metagenomic analysis revealed a significant reduction in microbial diversity (Chao index) in acne-affected skin compared to healthy controls (p < 0.001). The relative abundance of Staphylococcus, particularly Staphylococcus epidermidis, was significantly elevated in acne group (p < 0.05), while Cutibacterium acnes levels remained unchanged. Carbon metabolism pathways were enriched in the acne group (p < 0.05), predominantly driven by Cutibacterium, whereas other enriched metabolic pathways, such as ABC transporters and glycine, serine, and threonine metabolism (p < 0.05), showed a greater contribution from Staphylococcus. Virulence factors enriched in acne samples were primarily offensive in nature and largely attributed to Staphylococcus. Moreover, acne-associated microbiome exhibited a significantly higher prevalence of resistance genes against fluoroquinolones, fosfomycin, and triclosan (p < 0.05). Untargeted lipidomic analysis demonstrated significantly elevated total serum and triglyceride levels, along with a reduction in fatty acid chain length and a higher degree of saturation compared to the healthy group (p < 0.01). Specific triglycerides significantly enriched in the acne group, such as TG (15:0_14:0_16:0) + NH₄, exhibited a significant positive correlation with Staphylococcus. This correlation is associated with elevated clinical erythema and melanin indices, suggesting that Staphylococcus is implicated in the development of acne-related inflammation. Additionally, Thermus exhibits negative correlations with acne-associated lipids and inflammatory parameters, potentially exerting a protective role. These findings suggest that Cutibacterium and Staphylococcus play differential yet synergistic roles in acne pathogenesis. The observed skin microbiome dysbiosis and lipid metabolic alterations provide novel insights into the pathophysiology of acne vulgaris, which may inform the development of targeted therapeutic strategies.

Dental caries, a prevalent biofilm-mediated chronic disease, causes enamel demineralization, pulp infection, and systemic complications. Dental plaque biofilm is the initiating factor for the occurrence and development of caries. Streptococcus mutans is an opportunistic pathogen linked to the structure and ecology of dental plaque biofilms. The molecular mechanism of S. mutans during biofilm ontogeny in driving cariogenesis has been extensively elucidated. Here, we observed that asiatic acid is a potent biofilm disruptor that selectively dismantles S. mutans biofilm architectures, prompting us to investigate its mechanism. The minimum biofilm inhibition concentration (MBIC) of asiatic acid on S. mutans was 62.5 μM, but the MBIC level did not substantially impede planktonic growth. Using the static active-attachment model, it was demonstrated that asiatic acid significantly reduced biofilm biomass (p < 0.001) and extracellular polysaccharides (EPS) content (p < 0.001), while concurrently diminishing acid production (p = 0.017) and metabolic activity (p = 0.014). Confocal and scanning electron microscopy further confirmed structural disintegration, including bacterial detachment and reduced biofilm thickness. Transcriptome analysis of S. mutans biofilm treated with asiatic acid revealed 454 differentially expressed genes (adjusted p < 0.05, |log₂FC| ≥ 1). Notably, genes related to the CiaRH two-component system (ciaR, ciaH), a central regulatory hub for biofilm maturation and acid tolerance. This disruption initiates a downstream cascade, causing a coordinated downregulation of critical gene clusters essential for virulence and pathogenesis, including stress response (htrA, clpP, groEL, dnaK), and the glucan-binding protein gene (gbpC) essential for biofilm structural integrity. These findings provide the first mechanistic evidence linking asiatic acid to transcriptional reprogramming in S. mutans biofilm, offering a novel ecological strategy for caries prevention by targeting key regulatory pathways.

Hair loss is a complex multifactorial process. The mechanisms by which caffeine and adenosine act against hair loss have been extensively researched, but little is known about their effects on the microbiome and lipidome of the scalp. Hair loss may be associated with the status of scalp microbiota and lipids. Further investigation is warranted to determine whether caffeine and adenosine can regulate scalp microbiota and lipids and thus help to prevent hair loss. The objective of this study was to assess the effect of shampoo containing caffeine and adenosine on the scalp microbiome and lipidome in subjects experiencing hair loss who were aged between 18 and 60 years. The study was a randomized, single‐blind and parallel comparison trial involving full scalp treatment, which was conducted among 30 subjects experiencing hair loss. Samples were collected from subjects at baseline and at 12 weeks (±3 days). Microbiomes were analysed via 16S rDNA and ITS1 sequencing. Lipidome analysis was carried out using ultra‐high performance liquid chromatography–tandem mass spectrometry (UPLC‐MS/MS). At 12 weeks, significant clinical characteristics indicating an anti‐hair loss effect were evident. Abundances of Pseudomonas, Escherichia‐Shigella and Malassezia all decreased in the experimental group, whereas those of Talaromyces and Cutibacterium increased. In addition, levels of triglyceride (TG), diglyceride (DG), ceramide (Cer) and ceramide‐1‐phosphate (CerP) were all significantly impacted in the experimental group. Furthermore, abundances of lipid metabolites were tightly correlated with those of Escherichia‐Shigella and Talaromyces. Caffeine and adenosine may enhance the anti‐hair loss process through their effects on the lipidome and microbiome of the scalp.

Farms are a major source of antibiotic resistance genes (ARGs) and antibiotic-resistant bacteria (ARB), and previous research mainly focuses on polluted soils and breeding environments. However, slaughtering is an important link in the transmission of ARGs and ARB from farmland to dining table. In this study, we aim to reveal the pollution of ARGs and ARB in the slaughter process of broilers. First, by qualitative and quantitative analysis of ARGs in samples collected from the broiler slaughtering and processing production chain, the contamination level of ARGs was reflected; secondly, potential hosts for ARGs and microbial community were analyzed to reflect the possible transmission rules; thirdly, through the antibiotic susceptibility spectrum analysis of four typical food-borne pathogens, the distribution of ARB was revealed. The results showed that 24 types of ARGs were detected positive on the broiler slaughter production line, and tetracycline-resistance genes (20.45%) were the most frequently detected. The types of ARGs vary with sampling process, and all sampling links contain high levels of sul2 and intI1. The most abundant ARGs were detected in chicken surface in the scalding stage and entrails surface in the evisceration stage. There was a significant correlation between intI1 and tetM, suggesting that tetM might be able to enter the human food chain through class-1 integrons. The host range of the oqxB gene is the most extensive, including Sphingobacterium, Bacteroidia unclassified, Rothia, Microbacterium, Algoriella, etc. In the relevant links of the slaughter production line, the microbial community structure is similar. Removing viscera may cause diffusion of ARGs carried by intestinal microorganisms and contaminate chicken and following processing production. The four food-borne pathogens we tested are widely present in all aspects of the slaughter process, and most of them have multi-drug resistance and even have a high degree of resistance to some veterinary drugs banned by the Ministry of Agriculture. Our study preliminarily revealed the pollution of ARGs and ARB in the slaughter process of broilers, and these results are helpful to carry out food safety risk assessment and formulate corresponding control measures.

As an indispensable member of the family of lipid vitamins, vitamin K₂ (MK-7) plays an important role in blood coagulation, cardiovascular health, and kidney health. Microbial fermentation is favored due to its high utilization rate of raw materials, simple operation, and moderate conditions. However, the biosynthesis pathway of vitamin K₂ in microorganisms is highly complex, which hinders its industrial production in microbial cell factories. One of the major challenges is the stable expression and deregulation of key enzymes in the vitamin K₂ biosynthesis pathway, which remains unclear and has undergone little investigation. In this study, 2-succinyl-5-enolpyruvyl-6-hydroxy-3-cyclohexene-1-carboxylic-acid synthase (MenD) and 1,4-dihydroxy-2-naphthoate polyprenyltransferase (MenA) were identified as pivotal enzymes in the biosynthesis of vitamin K₂. To investigate the catalytic efficiency of MenD in the biosynthesis pathway of vitamin K₂, structure-based mutation design and site-directed mutagenesis were performed. Three mutation sites were identified in MenD: A115Y, R96 M, and R323M, which improve the expression level and protein stability. Meanwhile, the MenA mutant T290M, which exhibits improved protein stability, was obtained by modifying its hydrophobic stacking structure. Finally, an engineered strain noted ZQ13 that combinatorially overexpressed MenD (A115Y) and MenA (T290M) mutants was constructed and achieved 338.37 mg/L vitamin K₂ production in a 3-L fermenter.

The diversity and delicate balance of the oral microbiome contribute to oral health, with its disruption leading to oral and systemic diseases. Toothpaste includes elements like traditional additives such as sodium lauryl sulfate (SLS) as well as novel postbiotics derived from probiotics, which are commonly employed for maintaining oral hygiene and a healthy oral cavity. However, the response of the oral microbiota to these treatments remains poorly understood. In this study, we systematically investigated the impact of SLS, and toothpaste containing postbiotics (hereafter, postbiotic toothpaste) across three systems: biofilms, animal models, and clinical populations. SLS was found to kill bacteria in both preformed biofilms (mature biofilms) and developing biofilms (immature biofilms), and disturbed the microbial community structure by increasing the number of pathogenic bacteria. SLS also destroyed periodontal tissue, promoted alveolar bone resorption, and enhanced the extent of inflammatory response level. The postbiotic toothpaste favored bacterial homeostasis and the normal development of the two types of biofilms in vitro, and attenuated periodontitis and gingivitis in vivo via modulation of oral microecology. Importantly, the postbiotic toothpaste mitigated the adverse effects of SLS when used in combination, both in vitro and in vivo. Overall, the findings of this study describe the impact of toothpaste components on oral microflora and stress the necessity for obtaining a comprehensive understanding of oral microbial ecology by considering multiple aspects.

Background: The human skin microbiome and lipidome are essential for skin homeostasis and barrier function, and have become a focus in both dermatological and cosmetic fields. However, the influence of surfactants commonly used in cosmetic products on the skin resident microbiome and lipidome remains poorly characterized.Methods: We conducted self‐control experiments to systematically study the effects of surfactant (sodium lauroyl sarcosinate [SLS]) on facial skin. Wrinkles, pores, porphyrins, and superficial lipids were examined to evaluate the biophysical state of skin. Quantitative real‐time PCR was used to detect the numbers of bacteria and fungi. The diversity and structure of prokaryotic and eukaryotic microbiomes were assessed using 16S rDNA and ITS amplicon sequencing, respectively. Moreover, 22 lipids were identified to evaluate lipidome variations. SPSS software was used for statistical analysis.Results: SLS in facial cleanser did not extensively influence skin biophysical parameters, but caused a decrease in porphyrin. After using the SLS‐added facial cleanser for 3 weeks, the alpha diversity of the prokaryotic microbial community decreased significantly, while the eukaryotic microbial community showed a continuous downward trend but no statistically significant. A shift in the structure of prokaryotic microbiome was observed as a result of SLS exposure, mainly reflected by the increase in Acinetobacter, Escherichia‐Shigella, Streptococcus, and Ralstonia, while the SLS had little effect on the structure of the eukaryotic microbiome. Furthermore, SLS exposure had a great impact on skin lipidome, mainly manifested by the increase of phosphatidylglycerol (PG) and phosphatidylcholine (PC), and the decrease of ceramides. Spearman's correlations analysis showed that Escherichia‐Shigella, Pseudomonas, and Acinetobacter are positively correlated with PG and PC; however, the correlation is not statistically significant.Conclusion: In this study, we found the SLS in facial cleanser primarily affected lipidome and the prokaryotic microbiome of facial skin. These findings are useful for reminding us to be vigilant about the ingredients in personal care products, even the common ingredients, and designing effective formulations for repairing ecological balance of skin.