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E. hellem Ser/Thr protein phosphatase PP1 targets the DC MAPK pathway and impairs immune functions

Jialing Bao1,2, Yunlin Tang3,2, Yebo Chen3,2

  • 1The State Key Laboratory of Resource Insects, Southwest University, Chongqing, China baojl@swu.edu.cn.

Life Science Alliance
|January 10, 2024
PubMed

Insights

Microsporidia infections impair host dendritic cells (DCs), compromising immune responses. This study reveals Enterocytozoon hellem manipulates the p38α/NFAT5 pathway in DCs, highlighting a public health threat.

Area of Science:

  • Immunology
  • Cell Biology
  • Parasitology

Background:

  • Microsporidia infections are persistent and disrupt host cell functions.
  • Dendritic cells (DCs) are crucial for initiating adaptive immunity.
  • Enterocytozoon hellem is a common zoonotic microsporidia species.

Purpose of the Study:

  • To elucidate the impairing effects of microsporidia on host DCs.
  • To identify the molecular mechanisms underlying microsporidia-induced DC dysfunction.
  • To assess the impact of microsporidia on host immunity.

Main Methods:

  • In vivo mouse models to assess susceptibility to pathogenic challenges.
  • In vitro assays to evaluate DC immune functions (cytokine expression, maturation, phagocytosis, antigen presentation).
  • Molecular analysis of host-pathogen interactions, focusing on the MAPK pathway.

Main Results:

  • E. hellem infection increased host susceptibility and primarily affected DCs.
  • Infected DCs exhibited down-regulated cytokine expression, reduced maturation, phagocytosis, and antigen presentation.
  • E. hellem Ser/Thr protein phosphatase PP1 was found to interact with host p38α (MAPK14), manipulating the p38α/NFAT5 axis.

Conclusions:

  • E. hellem infection severely impairs DC immune functions, disrupting T cell priming and host immunity.
  • The study elucidates the molecular mechanism involving the p38α/NFAT5 pathway.
  • Microsporidiosis poses a significant threat to public health due to its impact on immune function.

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