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Background <p>The sterile alpha and HEAT/Armadillo motif (SARM) is the fifth Toll-like receptor (TLR) adaptor protein containing the Toll/interleukin-1 receptor (TIR) domain, which is highly enriched in the brain. <i>Toxoplasma gondii</i> (<i>T. gondii</i>) is an obligate intracellular parasitic protozoan that causes zoonotic toxoplasmosis, resulting in threats to human health, such as brain damage. Previous studies have shown that SARM plays crucial roles in cell death and triggers specific transcription programs of innate immunity in response to cell stress, viral, and bacterial infections. However, whether SARM is involved in <i>T. gondii</i> infection remains unclear.</p> Methods <p>In this report, quantitative real-time polymerase chain reaction (qPCR), western blot, flow cytometry, ethynyldeoxyuridine (EdU) assay, and enzyme-linked immunosorbent assay (ELISA) were used to explore the relationship between SARM and <i>T. gondii</i>.</p> Results <p>Here, we showed that <i>T. gondii</i> infection increased the expression of SARM in vitro and in vivo. SARM induced cell apoptosis during <i>T. gondii</i> infection, activating the mitochondrial apoptotic pathway, the endoplasmic reticulum stress (ER) pathway, and the mitogen-activated protein kinase (MAPK) signaling pathway, and prompting the production of reactive oxygen species (ROS). Furthermore, SARM participated in the regulation of the inflammatory response through the nod-like receptor pyrin domain 3 (NLRP3) inflammasome signaling pathway during <i>T. gondii </i>in vitro infection.</p> Conclusions <p>These results elucidate the relationship between SARM and <i>T. gondii</i> infection, suggesting that SARM may represent a potential target for <i>T. gondii</i> control.</p> Graphical Abstract <p></p>

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SARM regulates cell apoptosis and inflammation during Toxoplasma gondii infection through a multistep mechanism

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月12日

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  • Shumin Gao,
  • Min Gao,
  • Huanhui Du,
  • Lingyu Li,
  • Xudian An,
  • Yongyu Shi,
  • Xiaoyan Wang,
  • Hua Cong,
  • Bing Han,
  • Chunxue Zhou,
  • Huaiyu Zhou

摘要

Background

The sterile alpha and HEAT/Armadillo motif (SARM) is the fifth Toll-like receptor (TLR) adaptor protein containing the Toll/interleukin-1 receptor (TIR) domain, which is highly enriched in the brain. Toxoplasma gondii (T. gondii) is an obligate intracellular parasitic protozoan that causes zoonotic toxoplasmosis, resulting in threats to human health, such as brain damage. Previous studies have shown that SARM plays crucial roles in cell death and triggers specific transcription programs of innate immunity in response to cell stress, viral, and bacterial infections. However, whether SARM is involved in T. gondii infection remains unclear.

Methods

In this report, quantitative real-time polymerase chain reaction (qPCR), western blot, flow cytometry, ethynyldeoxyuridine (EdU) assay, and enzyme-linked immunosorbent assay (ELISA) were used to explore the relationship between SARM and T. gondii.

Results

Here, we showed that T. gondii infection increased the expression of SARM in vitro and in vivo. SARM induced cell apoptosis during T. gondii infection, activating the mitochondrial apoptotic pathway, the endoplasmic reticulum stress (ER) pathway, and the mitogen-activated protein kinase (MAPK) signaling pathway, and prompting the production of reactive oxygen species (ROS). Furthermore, SARM participated in the regulation of the inflammatory response through the nod-like receptor pyrin domain 3 (NLRP3) inflammasome signaling pathway during T. gondii in vitro infection.

Conclusions

These results elucidate the relationship between SARM and T. gondii infection, suggesting that SARM may represent a potential target for T. gondii control.

Graphical Abstract