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Background <p><i>Salmonella enterica</i> serovar <i>Typhimurium</i> is a gram-negative bacterium that infects intestinal cells, causing gastroenteritis in humans and animals. Following infection, the bacteria persist and replicate within a unique cytoplasmic compartment known as the <i>Salmonella</i>-containing vacuole. While the proliferation of most intracellular bacteria is restricted by classical autophagy, <i>Salmonella</i> has evolved mechanisms to evade autophagic intervention. Ubiquilin 1 (Ubqln1) contains an N-terminal ubiquitin-like domain and a C-terminal ubiquitin-associated domain. These domains play crucial roles in cellular protein degradation, autophagosome maturation, and the prevention of starvation-induced apoptosis.</p> Objective <p>This study investigates the regulation of Ubqln1 expression in response to <i>Salmonella</i> infection and elucidates the role of Ubqln1 in modulating <i>Salmonella</i> proliferation and the autophagic process.</p> Methods <p>To achieve this, we employed RT-PCR, Western blotting, a Ubqln1 overexpression system, and Ubqln1 knockout cell lines. Confocal microscopy was used to assess the spatiotemporal association between <i>Salmonella</i>, Ubqln1, and autophagic markers such as LC3.</p> Results <p>Our findings demonstrate that Ubqln1 expression is upregulated in response to treatment with major bacterial antigens (LPS, OmpA) or <i>Salmonella</i> infection. Intracellular proliferation of <i>Salmonella</i> was inhibited in cells overexpressing Ubqln1, whereas it was promoted in Ubqln1 deficient cells. Furthermore, Ubqln1 showed significant recruited to <i>Salmonella</i> and exhibited spatial overlap with the autophagy marker LC3, as confirmed by fluorescence intensity profiling. Notably, Ubqln1 appeared to inhibit the accumulation of LAMP2 around <i>Salmonella</i>.</p> Conclusion <p>Collectively, these results suggest that Ubqln1 plays a critical role in host defense against <i>Salmonella</i> by promoting Xenophagy.</p>

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Ubiquilin 1 Inhibits intracellular proliferation of Salmonella enterica serovar Typhimurium through Xenophagy

  • 期刊论文

  • 发表日期：

    2026年3月19日

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  • In Sook Jeon,
  • Yong-Hee Lee,
  • Jin Tae Hong,
  • Won Seop Kim,
  • Jae-Cheon Shin,
  • Hak-Kyo Lee,
  • Joong-Kook Choi

摘要

Background

Salmonella enterica serovar Typhimurium is a gram-negative bacterium that infects intestinal cells, causing gastroenteritis in humans and animals. Following infection, the bacteria persist and replicate within a unique cytoplasmic compartment known as the Salmonella-containing vacuole. While the proliferation of most intracellular bacteria is restricted by classical autophagy, Salmonella has evolved mechanisms to evade autophagic intervention. Ubiquilin 1 (Ubqln1) contains an N-terminal ubiquitin-like domain and a C-terminal ubiquitin-associated domain. These domains play crucial roles in cellular protein degradation, autophagosome maturation, and the prevention of starvation-induced apoptosis.

Objective

This study investigates the regulation of Ubqln1 expression in response to Salmonella infection and elucidates the role of Ubqln1 in modulating Salmonella proliferation and the autophagic process.

Methods

To achieve this, we employed RT-PCR, Western blotting, a Ubqln1 overexpression system, and Ubqln1 knockout cell lines. Confocal microscopy was used to assess the spatiotemporal association between Salmonella, Ubqln1, and autophagic markers such as LC3.

Results

Our findings demonstrate that Ubqln1 expression is upregulated in response to treatment with major bacterial antigens (LPS, OmpA) or Salmonella infection. Intracellular proliferation of Salmonella was inhibited in cells overexpressing Ubqln1, whereas it was promoted in Ubqln1 deficient cells. Furthermore, Ubqln1 showed significant recruited to Salmonella and exhibited spatial overlap with the autophagy marker LC3, as confirmed by fluorescence intensity profiling. Notably, Ubqln1 appeared to inhibit the accumulation of LAMP2 around Salmonella.

Conclusion

Collectively, these results suggest that Ubqln1 plays a critical role in host defense against Salmonella by promoting Xenophagy.