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Background <p><i>Salmonella</i> Typhimurium (STM) a gram negative, facultative, zoonotically important intracellular anaerobe causes nontyphoidal salmonellosis (NTS), which impacts huge economic losses in both veterinary and medical field. This bacterium manipulates various host processes, including host lipids metabolism for its survival. Nitrate anaerobic regulator L (NarL) is an important transcriptional regulator that mediates its pathogenesis under anaerobic conditions. However, the effect of narL on host lipid biogenesis is not well defined.</p> Methods and results <p>In this study, the effect of narL on lipid metabolism in murine macrophages infected with STM: Wild, STM: <i>ΔnarL</i>, and STM: <i>cnarL</i> was investigated. RAW264.7 macrophages infected with STM: <i>ΔnarL</i> exhibited 48.6% less lipid droplet (LD) accumulation at 6&#xa0;h, but 50% more than STM: WT at 24&#xa0;h. Further, quantification of LDs by thin layer chromatography (TLC) and high performance thin layer chromatography (HPTLC) showed significant accumulation of oleic acid among nonpolar lipids and phosphatidyl ethanolamine among polar lipids in infected murine macrophages. Quantification of enzymes involved in lipid metabolism by Real time PCR showed a significant upregulation (<i>P</i> ≤ 0.01) of <i>agpat1</i>, <i>fasn</i>, and <i>dgat1</i> at 6 hpi; however, <i>atgl</i>,<i> hsl</i>,<i> pla2</i>, and <i>pparα</i> were found to be upregulated at 24 hpi. Moreover, there was more survivability of STM in presence of oleic acid than phosphatidyl ethanolamine. However, STM: <i>ΔnarL</i> showed significantly decrease (<i>P</i> ≤ 0.01) in colony forming unit (CFU) as compared to STM: WT at each time point in presence of both polar and non polar lipid.</p> Conclusion <p>These finding suggests narL modulates lipid biogenesis inside the host cells. These observations provide an insight into the host pathogen interactions that would be targeted for developing new control strategies against salmonellosis.</p> Graphical Abstract <p></p>

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NarL gene modulates the host lipid metabolism for survival of Salmonella Typhimurium in murine macrophages

  • 期刊论文

  • 发表日期：

    2025年10月11日

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  • Pravas Ranjan Sahoo,
  • Ajay Kumar,
  • M. Pashupathi,
  • Karuna Irungbam,
  • Swagatika Priyadarsini,
  • Meeta Saxena,
  • Mukesh Kumar,
  • Mohini Saini

摘要

Background

Salmonella Typhimurium (STM) a gram negative, facultative, zoonotically important intracellular anaerobe causes nontyphoidal salmonellosis (NTS), which impacts huge economic losses in both veterinary and medical field. This bacterium manipulates various host processes, including host lipids metabolism for its survival. Nitrate anaerobic regulator L (NarL) is an important transcriptional regulator that mediates its pathogenesis under anaerobic conditions. However, the effect of narL on host lipid biogenesis is not well defined.

Methods and results

In this study, the effect of narL on lipid metabolism in murine macrophages infected with STM: Wild, STM: ΔnarL, and STM: cnarL was investigated. RAW264.7 macrophages infected with STM: ΔnarL exhibited 48.6% less lipid droplet (LD) accumulation at 6 h, but 50% more than STM: WT at 24 h. Further, quantification of LDs by thin layer chromatography (TLC) and high performance thin layer chromatography (HPTLC) showed significant accumulation of oleic acid among nonpolar lipids and phosphatidyl ethanolamine among polar lipids in infected murine macrophages. Quantification of enzymes involved in lipid metabolism by Real time PCR showed a significant upregulation (P ≤ 0.01) of agpat1, fasn, and dgat1 at 6 hpi; however, atgl, hsl, pla2, and pparα were found to be upregulated at 24 hpi. Moreover, there was more survivability of STM in presence of oleic acid than phosphatidyl ethanolamine. However, STM: ΔnarL showed significantly decrease (P ≤ 0.01) in colony forming unit (CFU) as compared to STM: WT at each time point in presence of both polar and non polar lipid.

Conclusion

These finding suggests narL modulates lipid biogenesis inside the host cells. These observations provide an insight into the host pathogen interactions that would be targeted for developing new control strategies against salmonellosis.

Graphical Abstract