Acne sequelae primarily include post-acne erythema, post-acne hyperpigmentation, and post-acne scarring. These residual cutaneous lesions persist in a substantial proportion of patients following the resolution of active acne and arise from factors such as inflammatory responses and inappropriate manipulation of lesions. Acne sequelae are highly prevalent, impose a considerable disease burden, and exert a profound negative impact on patients’ physical appearance, psychological well-being, and quality of life. Although a wide range of therapeutic modalities is currently available and new treatment technologies continue to emerge, substantial variability exists in treatment efficacy, and clinical decision-making remains highly heterogeneous. To promote standardized and evidence-based approaches to the diagnosis, prevention, and management of acne sequelae, an expert panel developed this consensus through a comprehensive review of recently published domestic and international literature, integrated with current clinical practice in China. This consensus is intended to provide practical and authoritative guidance for clinicians in the diagnosis, prevention, and treatment of acne sequelae.

Hidradenitis suppurativa (HS), also known as acne inversa (AI), is a chronic, recurrent inflammatory disease of the pilosebaceous unit that primarily affects intertriginous areas and is characterized by recurrent, painful, deep-seated inflammatory lesions. The pathogenesis of HS/AI is multifactorial, involving genetic susceptibility, immune dysregulation, microbial imbalance, and obesity. HS/AI remains difficult to manage, and current treatment aims to reduce the frequency and duration of flares, decrease disease severity, and improve quality of life. Treatment selection should be guided by disease severity and activity. Pharmacologic therapies include antibiotics, biologics, small-molecule agents, retinoids, and immunosuppressants, while adjunctive approaches include surgical interventions and energy-based therapies. This updated consensus aims to standardize the diagnosis and management of HS/AI in China and to improve clinical practice by providing a stepwise, multidisciplinary treatment framework in which interventions are stratified according to disease severity and recommendation strength. Recommendation strength was determined by expert voting: an agreement rate of ≥85% indicated “Should be recommended,” ≥75% to <85% indicated “Could be recommended,” ≥50% to <75% indicated “May be considered,” and <50% indicated “No consensus reached.” Key recommendations reaching the ≥85% agreement threshold included severity-based treatment selection, topical clindamycin for mild localized disease, systemic tetracyclines for mild-to-moderate HS/AI, and biologics, including adalimumab, secukinumab, and bimekizumab, for moderate-to-severe disease. The consensus has been registered on the International Practice Guidelines Registry Platform (No: PREPARE-2025CN1964).

Acne and hidradenitis suppurativa (HS) are inflammatory disorders of the pilosebaceous unit that exhibit distinct clinical manifestations, indicating that they likely differ in their underlying pathophysiology. Microbial dysbiosis is implicated in both diseases, yet direct comparisons using unified methods and analyses incorporating the oral microbiome are lacking. In this study, we collected lesional and nonlesional skin, buccal mucosa and faecal samples from 28 HS patients, 29 acne patients and 40 healthy controls, and profiled microbial communities using 16S rRNA V3-V4 sequencing with qPCR validation. HS lesions showed a pronounced enrichment of anaerobic Gram-negative taxa, including Prevotella, Porphyromonas and Fusobacterium, whereas acne lesions were dominated by Cutibacterium and Pseudomonas. Oral microbiome diversity was increased in both diseases, with HS showing distinct enrichment of Prevotella and Veillonella. HS patients also exhibited reduced gut microbial diversity. Correlation analyses revealed coordinated microbial alterations across the oral-gut-skin axis, and qPCR confirmed elevated concentrations of key anaerobes in HS. By directly comparing acne and HS across multiple anatomical sites, our study helps differentiate general inflammatory microbiome changes from those more specific to HS. The findings also suggest a potential oral-gut-skin microbial axis that may contribute to the chronic and destructive phenotype of HS, providing insights that could inform future microbiome-targeted therapeutic approaches.

Background:The clinical and laboratory characteristics of hidradenitis suppurativa (HS), particularly indicators related to disease severity, remain inadequately explored in Asian populations. Objectives:To characterize the clinical and laboratory features of HS in Chinese patients and to identify risk factors for disease severity. Methods:We retrospectively analyzed 197 patients with HS in China. Demographic, clinical, and laboratory data were collected. Disease severity was graded using the Hurley staging system. Comprehensive statistical analyses were conducted. Results:Among 197 patients, 87.8% were male (male-to-female ratio 7.2:1). Females had a shorter diagnostic delay than males (p = 0.011). Obesity was present in 33.0% of HS patients. Metabolic abnormalities included reduced HDL-c (30.0%), elevated blood glucose (29.1%), increased TG (14.93%), TC (10.31%), and LDL-c (8.96%). Neutrophil-related indices (WBC, ANC, NEUT%) and liver function markers (TP, albumin, ALT, AST, TB) were significantly associated with progression to Hurley stage III. ROC analysis showed modest discrimination for these indicators (AUCs, 0.605-0.652). In multivariable logistic regression analysis, TP remained an independent risk factor for progression to Hurley stage III (OR, 1.240; 95% CI, 1.101-1.397; p = 0.010). A multivariable logistic regression model that integrated significant predictors achieved an AUC of 0.689. This indicated moderate discrimination for advanced disease severity. Conclusion:Chinese patients with HS exhibited a pronounced male predominance and relatively mild metabolic abnormalities. Neutrophil-related indices and TP, especially when TP was interpreted together with albumin, were associated with progression to Hurley stage III.

Hidradenitis suppurativa (HS) is an autoinflammatory skin disease characterised by deep-seated and painful nodules, abscesses and draining tunnels that extensively penetrate the dermis in the axillae, inguinal and gluteal areas. The exact aetiology remains unclear. However, current evidence suggests that HS originates from an intrinsic defect within the hair follicle, leading to follicular obstruction, cyst development and eventual rupture, which triggers an inflammatory reaction. The initiation, progression and maintenance of the disease may involve functional abnormalities in keratinocytes (KCs), significantly contributing to the production of proinflammatory cytokines within and around the affected tissue and increased infiltration of immune cells. This review synthesises current evidence on KCs in HS, emphasising their genetic background and metabolic dysregulation. It comprehensively evaluates the cytokine milieu influenced by KCs within affected tissues. Notably, it highlights the diverse phenotypes of KCs within draining tunnels, underscoring their heterogeneity and implications for disease progression.

BackgroundHidradenitis suppurativa (HS) primarily occurs in intertriginous areas where apocrine sweat glands are densely distributed. The external ear, including ceruminous glands, a type of modified apocrine sweat gland, and its microbiome and lipidomic features, remains underexplored.ObjectiveTo investigate the clinical, histopathological, microbial, and lipidomic features of the external ear in HS.MethodsA cross-sectional study was conducted, collecting clinical, otoscopic, and histopathological data. The skin microbiome was analyzed via full-length 16S rRNA sequencing, and lipidomics was performed using UHPLC-MS/MS.Results65.2% of our patients presented with lesions in their external ears, most commonly hypertrophic scars. Pathogenic anaerobes, including Finegoldia magna and Peptoniphilus lacrimalis, exhibited higher abundance in HS, while the facultative anaerobe Fusicatenibacter was less abundant. Additionally, skin commensal bacteria, such as Cutibacterium acnes, were more prevalent in healthy controls (HCs). Staphylococcus auricularis was found to correlate with the cavum conchae involvement in HS. Moreover, HS exhibited marked differences in lipid metabolism, especially in glycerolipid, glycerophospholipid, and polyunsaturated fatty acid metabolism. Among them, S. auricularis was significantly negatively correlated with a cluster of triacylglycerols (TGs) and ceramides (Cers), while a significant positive correlation was observed with sphingomyelin (SM(d34:2)). Histopathology confirmed inflammation in the follicles and sebaceous glands, which was, however, sparse around ceruminous glands.ConclusionThe external ear may represent an underrecognized area of HS, sharing microbial and lipid metabolic alterations with typical HS skin lesions despite the absence of mechanical friction. HS primarily affects pilosebaceous units, while apocrine sweat glands may be involved as a standby.

BACKGROUND:The efficacy and safety of botulinum toxin type A (BoNTA) treatment for primary axillary hyperhidrosis (PAH) have not been explored in the Chinese population. OBJECTIVES:The objective was to evaluate efficacy and safety of 1 intradermal BoNTA injection in Chinese PAH cases. METHODS:This was a Phase 3, multicenter, randomized, double-blind, placebo-controlled study. Patients were randomized to an experimental group or the control group at a ratio of 3:1 and received either BoNTA or a placebo once. The primary efficacy endpoint was the proportion of patients who experienced an over 50% reduction in axillary sweat weight at Week 4 posttreatment compared to baseline. The key secondary efficacy endpoints were the percentage changes in axillary sweat weight at Weeks 1, 4, 8, and 16 posttreatment. RESULTS:A total of 344 patients were randomized to the experimental group (n = 258) or the control group (n = 86). The proportions of patients who experienced an over 50% reduction in axillary sweat weight at Week 4 posttreatment were 83.72% (216/258) in the experimental group and 55.81% (48/86) in the control group, respectively. The between-group difference was 27.91% (P < .001). BoNTA treatment yielded a significant reduction in axillary sweat weight, hyperhidrotic area, hyperhidrosis disease severity scale (HDSS) scores, and grade of bromhidrosis. The patients in the experimental group reported significantly higher satisfaction scores than those in the control group. BoNTA treatment was well tolerated. Neither group experienced suspected unexpected serious adverse reactions, or adverse events or adverse drug reactions leading to withdrawal or death. CONCLUSIONS:One intradermal 50-U BoNTA treatment led to a significant reduction in axillary sweat weight, axillary hyperhidrotic area, HDSS scores, and axillary bromhidrosis grades in Chinese PAH patients. The therapeutic effect was maintained for 16 weeks posttreatment, with a favorable safety profile. LEVEL OF EVIDENCE: 1 (THERAPEUTIC):

Lentigo simplex is a benign melanocytic lesion commonly arising in childhood. We report a 10-year-old girl with a stable periorbital lentigo simplex treated using a 755-nm picosecond alexandrite laser. The patient underwent five treatment sessions over three years, resulting in significant pigment reduction without adverse effects or recurrence. This case highlights the long-term safety and efficacy of picosecond laser treatment for pediatric facial pigmented lesions, particularly in cosmetically sensitive areas. It also adds to the limited literature supporting laser use in children and emphasizes the importance of noninvasive options for aesthetic concerns.

Ultraviolet (UV) irradiation leads to acute photodamage, photoaging and skin cancers. Post-translational modifications (PTMs) represent a key regulatory layer by modulating protein function, localization and interactions under UV stress. This review discusses the mechanistic involvement of PTMs in UV-induced skin damage and summarizes emerging PTM-related photoprotective strategies. Phosphorylation is a central mediator of UV-induced signal transduction, driving activation of the epidermal growth factor receptor (EGFR) and its downstream signalling pathways. Acetylation exerts distinct regulatory effects: histone acetylation primarily regulates transcription of inflammation-related genes and matrix metalloproteinases (MMPs), while non-histone acetylation modulates cellular senescence and mitochondrial antioxidant defence through modification of key proteins. Ubiquitination regulates protein degradation and, through non-degradative modifications, participates in DNA damage recognition and nucleotide excision repair (NER). Furthermore, other PTMs, including methylation, glycosylation, citrullination, SUMOylation and poly(ADP-ribosyl)ation (PARylation), participate in diverse regulatory processes during UV-induced cutaneous alterations. Experimental and emerging interventions associated with PTMs in UV-induced skin damage range from natural extracts to small-molecule agents and mainly include upstream-level modulation of oxidative stress, metabolic status or key effector protein function, as well as enzyme-level modulation of PTM writers and erasers. Different classes of PTMs contribute to UV-induced skin damage through distinct regulatory mechanisms. Further studies should explore the roles of emerging and less-characterized PTMs and evaluate interventions targeting PTM-regulating enzymes in physiologically relevant skin models.

BACKGROUND:Conventional botulinum toxin type A (BoNT/A) products include non-therapeutic accessory proteins vary in composition and manufacturing processes, which may contribute to differences in purity and biochemical characteristics. YY001 (Retoxin®) is a novel recombinant BoNT/A manufactured via E. coli expression to reduce impurities, improve purity, and minimize immunogenic risk. OBJECTIVES:To evaluate the efficacy, safety, and immunogenicity of YY001, a recombinant botulinum toxin type A (Chongqing Claruvis Pharmaceutical Co., Ltd., Chongqing, China), in the treatment of moderate-to-severe glabellar lines. METHODS:In this multicenter, randomized, double-blind, vehicle- and active-controlled Phase III trial, 529 adults aged 18-65 with moderate to severe glabellar lines were randomized 4:2:1 to receive a single 20 U injection of YY001, Botox®(Allergan Pharmaceuticals Ireland, Westport, Ireland), or vehicle. The primary endpoint was composite response rate (CRR) at Week 4, defined as a ≥2-grade improvement of glabellar line severity assessed by both investigator and participant. Secondary endpoints included onset time, duration, satisfaction, and safety. RESULTS:YY001 achieved a CRR of 86.7% at Week 4, significantly outperforming Botox® (66.7%, P < .0001) and vehicle (1.3%, P < .0001). It showed faster onset, longer median duration (97 days), and high participant satisfaction. Adverse events were mild and comparable across groups. Only one case of anti-drug antibody was observed; no neutralizing antibodies were detected. A 12-week follow-up and ethnically homogenous population may limit generalizability. CONCLUSIONS:YY001 demonstrated strong efficacy and a favorable safety profile than Botox®. Longer-term and multicenter studies are needed to assess durability, immunogenicity, and applicability across broader populations. LEVEL OF EVIDENCE: 1 (THERAPEUTIC):For image description, please refer to the figure legend and surrounding text.

BACKGROUND:Ultraviolet (UV) radiation contributes to premature skin aging, and sirtuin 6 (SIRT6) plays key roles in aging, genomic stability, inflammation, and metabolism. However, the specific role of SIRT6 in UV-induced photoaging remains unclear. OBJECTIVE:To investigate the role of SIRT6 in UVB-induced skin photoaging and uncover the molecular mechanisms underlying its regulation. METHODS:A UVB-induced photoaging mouse model was established, and the role of SIRT6 was determined in vivo using histopathological and transcriptomic analyses. Candidate miRNAs targeting SIRT6 were predicted using bioinformatics tools and validated using dual-luciferase reporter assays. SIRT6 protein levels were measured via western blotting, and miRNA expression was analyzed via quantitative real-time polymerase chain reaction. Functional assays were conducted using human dermal fibroblasts (HDF) to assess cellular senescence, reactive oxygen species (ROS) production, and DNA damage. RESULTS:SIRT6 deficiency substantially exacerbated UVB-induced skin aging, characterized by collagen degradation, elastin fragmentation, and dermal structure loss. Moreover, miR-663a and miR-4706 directly targeted the 3'-untranslated region of SIRT6 and were upregulated in HDFs after UVB exposure. Overexpression of these miRNAs promoted HDFs senescence, DNA damage, and ROS accumulation, thus mirroring the effects of SIRT6 silencing. Furthermore, SIRT6 was confirmed as a key regulator of the gene networks involved in skin immune responses and inflammation following chronic UVB exposure. CONCLUSION:The study enriches existing knowledge regarding the molecular connections between miRNAs and SIRT6. Moreover, the study provides new insights into miRNA-mediated SIRT6 regulation and proposes an intervention point for the prevention of UVB-induced photoaging and age-related diseases.

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disorder, affecting the pilosebaceous unit in apocrine gland-rich areas, characterized by painful nodules, abscesses and draining tunnels. The underlying molecular and immunological mechanisms remain poorly understood. This study aimed to identify key gene expression patterns, hub genes, and analyze the potential role of the CCL19/CCL21-CCR7 axis in HS lesions and peripheral blood using bulk and single-cell RNA sequencing analyses. By employing an integrative approach that included three machine learning methods and subsequent validation on an independent dataset, we successfully identified AKR1B10, IGFL2, WNK2, SLAMF7, and CCR7 as potential hub genes and therapeutic targets for HS treatment. Furthermore, our study found that CCL19 and CCL21 may originate from various cells such as fibroblasts and dendritic cells, playing a crucial role in recruiting CCR7-associated immune cells, particularly Treg cells. The involvement of the CCL19/CCL21-CCR7 axis in HS pathogenesis suggests that other CCR7-expressing cells may also be recruited, contributing to disease progression. These findings significantly advance our understanding of HS pathogenesis offer promising avenues for future CCR7-targeted therapeutic interventions.

Tissue-resident memory T cells (TRM) play a pivotal role in skin immunity, serving not only as key mediators of local immune defense but also as contributors to the onset, persistence, and recurrence of chronic inflammatory skin diseases. Recent studies have identified TRM as major drivers of disease relapse and chronic maintenance. This review summarizes the mechanisms underlying differentiation, residency, and survival of TRM in the skin, with an emphasis on their subset heterogeneity and tissue-specific regulation. We further highlight recent evidence of TRM pathogenicity in representative diseases such as psoriasis, vitiligo, and atopic dermatitis, paying particular attention to their unique role in disease recurrence. In addition, we discuss how current therapeutic interventions may influence TRM development and survival. A deeper understanding of the dual roles of TRM will provide new insights and potential breakthroughs for the precise management of chronic inflammatory skin diseases.

The 755-nm picosecond laser device has undergone recent updates. A comprehensive evaluation is warranted to summarize and recognize efficacy and safety profiles of the 755-nm picosecond laser with a novel platinum focus lens array for skin lightening and rejuvenation. A retrospective analysis was conducted on patients who received treatment with the updated 755-nm picosecond laser device. Standardized clinical photographs were taken prior to treatment and during follow-up assessments. A modified global aesthetic improvement scale was employed as the main evaluation indicator. Additionally, the abdomens of 4-week-old Bama miniature pigs were treated with the new laser device. Histological changes were examined using hematoxylin and eosin staining, Masson's Trichrome staining, and immunohistochemical techniques. The study involved 10 patients with Fitzpatrick skin types IV to V, presenting with wrinkles, enlarged pores, and pigmented lesions. Notable improvements were observed, accompanied by minimal downtime and complications. Histological analysis conducted immediately after treatment revealed the presence of vacuoles within the epidermis and extravasation of red blood cells in the superficial dermis. Furthermore, dermal thickness exhibited a significant increase following treatment across all energy settings. The expression of collagen type I proteins also showed an increase post-treatment with the new device. The newly developed 755-nm picosecond laser device effectively induces laser-induced optical breakdown and initiates dermal remodeling. It represents a safe and effective therapeutic option for facial rejuvenation.

BACKGROUND:Ultraviolet (UV) B can reach the epidermis and superficial dermis of the skin, inducing sunburn, inflammation, immunosuppression, cancer, and so on. Our former research found that receptor interacting protein (RIP) 1 could be upregulated in human dermal fibroblasts(HDFs) after UVB irradiation by using two-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization time of flight mass spectrometry techniques. Besides, our further research found that RIP1 was involved in the UVB-induced production of ROS and MMPs in HDFs. So far, the mechanisms of skin photodamage induced by UV mainly include DNA damage, oxidative stress, inflammation, apoptosis, and necroptosis. The NF-κB pathway can be activated eventually in the occurrence of inflammation and thus produce inflammatory cytokines such as IL-1, TNF-α, IL-6, and IL-8. However, the mechanism by which the upregulation of RIP 1 induced by UVB contributes to photodamage is still unclear. AIMS:To explore the role of RIP1 in UVB-induced skin inflammation and the related signal pathways and molecular mechanism, thus providing possible molecular markers for the diagnosis and prevention of skin photodamage. METHODS:Human dermal fibroblasts were cultured in vitro from normal human skin tissues. Besides, HaCaT cell lines and Balb/c nude mice were also the research objects. First, cellular models of UVB-induced upregulation of RIP1 were established. Then, the expression of RIP1 and localization of RIP1 before and after UVB irradiation of the cells were studied through western blot and immunofluorescence. Then, the change in the expression of the nuclear factor (NF)-kappaB (NF-κB) pathway, along with RIP1 in these cells before and after UVB irradiation was detected, including NF-κB p50/p65, p-p65, IκB and cytokines such as IL-1, IL-6, IL-8, and TNF-α. Next, the effects of the RIP1 inhibitor Nec-1 and RIP1 siRNA on the expression of RIP1, p-RIP1, NF-κB p50/p65, inflammatory cytokines, and nuclear translocation of p-p65 in vitro cells after UVB irradiation were explored. At last, the expression of RIP1 and NF-κB pathway-related proteins such as p65/p50 was detected by western blot and immunohistochemistry before and after UVB radiation with or without subcutaneous injection of Nec-1 in the Balb/c nude mice were detected. RESULT:We provide that RIP1 involved in the photodamage of human dermal fibroblasts, HaCaT cell lines, and the skin tissues of Balb/c nude mice induced by UVB. Upregulated RIP1 induced by UVB ultimately upregulates inflammatory cytokines, including IL-1, IL-6, IL-8, and TNF-α by triggering the expression of NF-κB p65/p50 and activating nuclear translocation of p-p65 in cells. RIP1 inhibitor Nec-1 or RIP1 siRNA can inhibit the function of RIP1. We first illustrate that the upregulated RIP1 induced by UVB contributes to photodamage of the skin via the NF-κB signaling pathway in vivo and in vitro. CONCLUSION:The study reveals the molecular mechanism by which upregulated RIP induced by UVB contributes to the occurrence of inflammation of the skin and also provides possible molecular markers for the diagnosis and prevention of skin photodamage.

Hidradenitis suppurativa (HS), also known as acne inversa, is a chronic inflammatory skin disorder characterized by recurrent inflammatory nodules, abscesses, sinus tracts (tunnels), and hypertrophic scarring. The condition often causes significant psychological distress and markedly reduces quality of life. Although its pathogenesis remains incompletely understood, multiple contributing factors—including genetic predisposition, immune dysregulation, hormonal influences, and lifestyle factors—have been implicated. The disease’s recurrence, complexity, and poorly defined pathogenesis make effective treatment particularly challenging. While lifestyle modifications, weight loss, smoking cessation, topical therapies, and oral antibiotics may be effective in mild cases, moderate-to-severe HS remains difficult to manage. This narrative review summarizes recent advances in therapeutic strategies for HS based on published literature and clinical trials. Our goal is to update clinicians on current treatment developments and support improved disease management to enhance the quality of life for individuals affected by HS.

Ultraviolet B (UVB) is recognized for inducing inflammation and death of keratinocytes through the activation of death receptors and pattern recognition receptors (PRRs). Receptor-interacting protein kinase 1 (RIPK1) and RIPK3 play pivotal roles in mediating necroptosis, which can be triggered by the activation of specific death receptors and PRRs. In this study, we observed a reduction of RIPK1 protein after UVB exposure which led to activation of Nuclear factor-kappa B (NF-κB) in HaCaT cells. This activation, in turn, promoted the production of IL-1β and TNF-α. However, RIPK1 kinase remained inactive and did not participate in cell death. Interestingly, UVB radiation triggered the activation of RIPK3 independently of RIPK1 kinase activity and subsequently induced phosphorylation of mixed-lineage kinase domain-like protein (MLKL), culminating in necroptosis and inflammation of the skin. At the same time, UVB-induced activation of RIPK3 also played a role in promoting the mitochondrial apoptotic pathway of Keratinocytes. In conclusion, UVB irradiation initiates an inflammatory response via RIPK1 pathway without necessitating its enzymatic activity. Simultaneously, RIPK3 can be activated by UVB exposure independently of RIPK1’s activity, resulting in necroptosis and inflammation of the skin.

The degree of severity varies greatly among different patients with acne inversa(AI)/hidradenitis suppurativa(HS),and disease severity usually determines treatment strategies.There have been a number of severity assessment criteria for AI/HS,such as the Hurley grading system,Sartorius score,HS severity index,etc.,which have been widely used in clinical classification and research and have shown clinical guiding significance.However,limitations still exist in some criteria,such as low sensitivity for efficacy evaluation,limited application range,etc.This review introduces several severity assessment criteria for AI/HS that have been proposed in recent years,aiming to better evaluate the disease and carry out graded treatment.

Abstract Objective: Hidradenitis Suppurativa (HS) underlying molecular and immunological mechanisms remain poorly understood. This study aimed to unravel key gene expression patterns, identify hub genes, and analyze immune cell infiltration in HS lesions and peripheral blood. Methods: Peripheral blood and skin tissues of HS datasets were sourced from the GEO database. The dataset with the larger sample size served as the training set to identify differential genes (DEGs) between HS patients and healthy controls. Hub genes were identified using the random forest (RF), LASSO logistic regression, and support vector machine-recursive feature elimination (SVM-RFE) algorithms. Additionally, CIBERSORT was employed to determine the proportions of 22 immune cell types in HS patients and to assess their correlation with the identified hub genes. Finally, the application of single-cell RNA-seq analysis serves to enhance and refine our comprehension of the cellular heterogeneity present in HS lesions. Results: In HS skin lesion samples, we identified reliable 200 DEGs: 141 were upregulated, and 59 were downregulated by three methods (limma, DESeq2, and edgeR). Similarly, in blood samples associated with HS, we screened132 DEGs, with 67 upregulated and 65 downregulated genes. Through an integrative approach involving three machine learning methods and subsequent validation on an independent dataset, we successfully identified AKR1B10, IGFL2, WNK2, SLAMF7, and CCR7 as potential biomarkers and therapeutic targets for HS treatment. Furthermore, immune cell infiltration analysis showed that HS is marked by dysregulations in multiple immune cells, and correlations exist between diverse immune cells, hub genes, and immune cell subsets. Conclusion: AKR1B10, IGFL2, WNK2, SLAMF7, and CCR7 were successfully identified. Single-cell RNA-seq analysis further refines our understanding of the cellular heterogeneity in HS lesions. These findings contribute to advancing our knowledge of HS pathogenesis and hold promise for future therapeutic interventions.

BackgroundAcne inversa (AI) is a refractory inflammatory skin disease, and TNF-α plays an important role in the pathogenesis of AI. By blocking TNF-α, infliximab (IFX) has been proven to be a promising method.ObjectivesTo explore the underlying mechanisms of IFX treatment in AI patients.MethodsIn this research, we integrated transcriptome sequencing data from the samples of our patients with AI and the GEO database. Ex vivo skin culture of AI patients was conducted to evaluate the efficacy of IFX treatment. Animal studies and cell experiments were used to explore the therapeutic effect and mechanism of IFX treatment.ResultsBoth TNF-α and NLRP3 inflammasome-related pathways were enriched in skin lesions of AI patients and murine AI models. After IFX treatment, the NLRP3 inflammasome-related pathway was effectively blocked, and the IL-1β level was normalized in ex vivo AI skin explants and murine AI models. Mechanistically, IFX suppressed the NF-κB signaling pathway to lower the expression of NLRP3 and IL-1β in keratinocytes.ConclusionsIFX treatment alleviated skin lesions in murine AI models and downregulated NLRP3 and IL-1β expression levels by inhibiting the NF-κB signaling pathway, which was helpful for understanding the mechanism of IFX therapy.