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<p>Ultraviolet B (UVB) exposure initiates skin carcinogenesis by generating persistent DNA photolesions and immunosuppressive microenvironment. Whether a defined probiotic can reinforce genome maintenance while counteracting UVB-driven inflammatory–checkpoint programs remains unclear. Here we show that oral administration of <i>Lactiplantibacillus plantarum</i> TH-B59 accelerates cyclobutane pyrimidine dimers (CPDs) resolution and dampens γ-H2AX accumulation in UVB-irradiated BALB/c skin. TH-B59 restores the expression of nucleotide excision repair–related genes (<i>Xpc</i>, <i>Ercc4</i>, <i>Xpa</i>, and <i>Ercc5</i>) and attenuates UVB-induced PI3K/AKT signaling. In parallel, TH-B59 suppresses UVB-induced NF-κB/COX-2/PGE<sub>2</sub> activation, reduces PD-L1 induction, and enhances IL-12 transcription, consistent with a shift toward immune surveillance. Fecal microbiota profiling identifies UVB-associated dysbiosis and a TH-B59–linked microbiome reconfiguration, with integrative correlation/network analyses connecting <i>L. plantarum</i> abundance to increased NER gene expression and reduced inflammatory mediators across gut and skin. Whole-genome sequencing supports TH-B59 as a bacteriocin-encoding, stress-tolerant strain lacking transferable antibiotic resistance and virulence determinants. Collectively, TH-B59 couples photolesion clearance with inflammatory–checkpoint remodeling to mitigate early UVB programs that drive photocarcinogenesis.</p>

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Oral Lactiplantibacillus plantarum accelerates nucleotide excision repair and suppresses UVB-induced checkpoint immunosuppression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月29日

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  • Qiwen Zheng,
  • Trang Thi Minh Nguyen,
  • Yoon-Soo Gwak,
  • Seul-Yi Lee,
  • Jae-Woo Kim,
  • Gyeong-Seon Yi,
  • Jin-Woo Choi,
  • So-Hee Chun,
  • Ye-Rim Choi,
  • Chan-Il Bae,
  • Jeehaeng Jeong,
  • Jaeyoung Choi,
  • Mi-Ju Kim,
  • Soo-Jin Park,
  • Tae-hoo Yi

摘要

Ultraviolet B (UVB) exposure initiates skin carcinogenesis by generating persistent DNA photolesions and immunosuppressive microenvironment. Whether a defined probiotic can reinforce genome maintenance while counteracting UVB-driven inflammatory–checkpoint programs remains unclear. Here we show that oral administration of Lactiplantibacillus plantarum TH-B59 accelerates cyclobutane pyrimidine dimers (CPDs) resolution and dampens γ-H2AX accumulation in UVB-irradiated BALB/c skin. TH-B59 restores the expression of nucleotide excision repair–related genes (Xpc, Ercc4, Xpa, and Ercc5) and attenuates UVB-induced PI3K/AKT signaling. In parallel, TH-B59 suppresses UVB-induced NF-κB/COX-2/PGE2 activation, reduces PD-L1 induction, and enhances IL-12 transcription, consistent with a shift toward immune surveillance. Fecal microbiota profiling identifies UVB-associated dysbiosis and a TH-B59–linked microbiome reconfiguration, with integrative correlation/network analyses connecting L. plantarum abundance to increased NER gene expression and reduced inflammatory mediators across gut and skin. Whole-genome sequencing supports TH-B59 as a bacteriocin-encoding, stress-tolerant strain lacking transferable antibiotic resistance and virulence determinants. Collectively, TH-B59 couples photolesion clearance with inflammatory–checkpoint remodeling to mitigate early UVB programs that drive photocarcinogenesis.