Injectable skin boosters currently in use mainly provide short-lived volumization or depend on inflammation-mediated collagen stimulation, raising concerns regarding durability and safety. Injectable particulate human acellular dermal matrix (phADM) is a biologically derived extracellular matrix scaffold designed to support constructive dermis remodeling. This randomized, split-face, double-blinded clinical trial evaluated the efficacy of phADM as a facial skin booster in 20 adults with moderate cheek roughness. phADM was injected on one facial side, with hyaluronic acid serving as the contralateral control. Multiple skin parameters were assessed over 20 weeks using validated imaging and biophysical instruments. Mechanistic validation was conducted using complementary in vitro, ex vivo human skin, and in vivo rat models. Clinically, the phADM-treated side demonstrated greater improvements in skin density, volume, elasticity, wrinkle depth, pore area, hydration, and barrier-related parameters at multiple time points compared with HA. In ex vivo human skin, phADM showed homogeneous dermal distribution and preservation of extracellular matrix architecture, along with restoration of basement membrane-associated proteins following UVB irradiation. In vivo rat studies revealed fibroblast infiltration and localized neocollagenesis within the implanted matrix. In vitro assays further indicated enhanced fibroblast proliferation and extracellular matrix synthesis, increased hyaluronan production, suppression of pro-inflammatory cytokines in activated macrophages, and downregulation of melanogenesis-related genes in melanoma cells. No serious adverse events were observed during the clinical study. These findings indicate that phADM functions as a restorative skin booster that promotes durable dermis remodeling and functional rejuvenation with a favorable safety profile.

Acne vulgaris is a chronic inflammatory dermatosis where conventional therapies often face limitations in efficacy and safety, necessitating the development of microbiome-targeted interventions. This study investigated the immunomodulatory potential of microbiome-derived tryptophan metabolites as a novel therapeutic strategy for Cutibacterium acnes (C. acnes)-induced inflammation, focusing on the aryl hydrocarbon receptor (AHR) pathway. We evaluated indole-3-lactic acid (ILA), indole-3-acrylic acid (IAA), and indole-3-propionic acid (IPA) in comparison to tapinarof, utilizing C. acnes-stimulated human epidermal keratinocytes and a C. acnes-induced acne mouse model. In vitro, ILA and IPA significantly suppressed C. acnes-driven inflammatory mediators, including Tumor Necrosis Factor-alpha (TNF-α), Interleukin (IL)-1β, and Cyclooxygenase-2 (COX2), whereas IAA demonstrated limited efficacy. In vivo, ILA treatment exhibited superior therapeutic activity, markedly reducing inflammatory cell infiltration, epidermal hyperplasia, and IL-1β expression. Transcriptomic analysis confirmed that ILA attenuates inflammatory signaling (e.g., IL-17 and TNF pathways) while upregulating AHR-responsive genes such as Cytochrome (CYP) 1A1 and CYP1B1. Collectively, these findings establish ILA as a potent postbiotic that mitigates cutaneous inflammation through selective activation of the AHR. Future studies should prioritize the clinical translation of ILA-based topical formulations, with rigorous evaluation of their efficacy and safety in well-designed human trials, to support their development as a non-antibiotic therapeutic alternative for acne management.

Keloids are fibroproliferative skin tumors characterized by excessive collagen deposition and persistent inflammation. Interleukin (IL)-6 plays a key role in wound healing and fibrosis, and promoter polymorphisms of the IL-6 gene have been implicated in keloid susceptibility in several populations. However, data on Vietnamese patients remain limited. We conducted a case-control study including 47 patients with clinically diagnosed keloids and 43 age- and sex-matched healthy controls to investigate the association between the IL-6 rs1800796 (−572 C>G) polymorphism and both keloid susceptibility and scar severity. Genotyping was performed using allele-specific oligonucleotide – polymerase chain reaction (ASO-PCR). Scar severity was assessed using the Vancouver Scar Scale (VSS). The CG genotype and G allele were significantly more frequent in patients with keloid than in controls. Carriers of the G allele demonstrated an increased risk of keloid formation and exhibited progressively higher VSS scores compared with CC homozygotes. These findings suggest that the IL-6 rs1800796 G allele is associated with increased susceptibility to keloids and greater scar severity in Vietnamese patients.