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Background <p>Disruption of the intestinal epithelial barrier is a hallmark of inflammatory bowel disease (IBD). Although probiotics and postbiotics are increasingly recognized as potential therapeutic approaches, treatment efficacy is often influenced by patient-specific variability.</p> Methods <p>In this study, intestinal inflammation was modeled by exposing HT-29 cells to fecal supernatants (FS) derived from three patients with ulcerative colitis (UC). The expression of pro-inflammatory (<i>IL-8</i>) and barrier-associated (<i>Claudin-1</i>, <i>MUC2</i>) genes was assessed by real-time PCR. Subsequently, the restorative effects of different preparations of <i>Lactobacillus helveticus</i> SBT2171, including live bacteria, cell-free supernatant, and debris-containing supernatant, were evaluated at 24 and 48&#xa0;h.</p> Results <p>FS exposure significantly upregulated <i>IL-8</i> expression while downregulating <i>Claudin-1</i> and <i>MUC2</i>, thereby recapitulating IBD-associated epithelial disruption. Treatment with <i>L. helveticus</i> preparations partially restored barrier-related gene expression in a patient- and treatment-dependent manner. Live bacteria induced transient or sustained <i>Claudin-1</i> upregulation depending on the FS source, whereas the cell-free supernatant demonstrated broader and more durable restorative effects across distinct inflammatory contexts. In contrast, debris-containing preparations exerted limited or even suppressive effects, particularly on <i>MUC2</i> expression.</p> Conclusions <p>These findings demonstrate that the barrier-restorative effects of <i>L. helveticus in vitro</i> is not uniform but shaped by the unique inflammatory and microbial environment of each patient. Collectively, our results support the potential of postbiotic formulations as safer and effective modulators of epithelial barrier repair and underscore the need for personalized strategies in microbiota-based therapies for IBD.</p>

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Personalized barrier recovery induced by Lactobacillus helveticus SBT2171 in an In Vitro model of ulcerative colitis-derived fecal supernatants

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月23日

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  • Melika Khademi,
  • Nesa Kazemifard,
  • Mohadese Fathi,
  • Maryam Farmani,
  • Shaghayegh Baradaran Ghavami,
  • Binazir Khanabadi,
  • Shabnam Shahrokh

摘要

Background

Disruption of the intestinal epithelial barrier is a hallmark of inflammatory bowel disease (IBD). Although probiotics and postbiotics are increasingly recognized as potential therapeutic approaches, treatment efficacy is often influenced by patient-specific variability.

Methods

In this study, intestinal inflammation was modeled by exposing HT-29 cells to fecal supernatants (FS) derived from three patients with ulcerative colitis (UC). The expression of pro-inflammatory (IL-8) and barrier-associated (Claudin-1, MUC2) genes was assessed by real-time PCR. Subsequently, the restorative effects of different preparations of Lactobacillus helveticus SBT2171, including live bacteria, cell-free supernatant, and debris-containing supernatant, were evaluated at 24 and 48 h.

Results

FS exposure significantly upregulated IL-8 expression while downregulating Claudin-1 and MUC2, thereby recapitulating IBD-associated epithelial disruption. Treatment with L. helveticus preparations partially restored barrier-related gene expression in a patient- and treatment-dependent manner. Live bacteria induced transient or sustained Claudin-1 upregulation depending on the FS source, whereas the cell-free supernatant demonstrated broader and more durable restorative effects across distinct inflammatory contexts. In contrast, debris-containing preparations exerted limited or even suppressive effects, particularly on MUC2 expression.

Conclusions

These findings demonstrate that the barrier-restorative effects of L. helveticus in vitro is not uniform but shaped by the unique inflammatory and microbial environment of each patient. Collectively, our results support the potential of postbiotic formulations as safer and effective modulators of epithelial barrier repair and underscore the need for personalized strategies in microbiota-based therapies for IBD.