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Giardia duodenalis MIF induces host intestinal damage via CD74 receptor mediated NLRP3 inflammasome activation

Mengge Chen1, Jianhua Li1, Xiaocen Wang1

  • 1State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun, China.

Plos Neglected Tropical Diseases
|February 2, 2026
PubMed

Insights

Giardia duodenalis MIF (GdMIF) activates the NLRP3 inflammasome via CD74 interaction, causing intestinal damage. Inhibiting this pathway reduces inflammation and protects against giardiasis.

Area of Science:

  • Immunology
  • Parasitology
  • Molecular Biology

Background:

  • Giardia duodenalis causes global public health issues through diarrhea.
  • Macrophage migration inhibitory factor (MIF) mediates immune responses; parasite-derived MIF's role in disease is unclear.
  • The specific function of G. duodenalis MIF (GdMIF) in giardiasis pathogenesis requires elucidation.

Purpose of the Study:

  • To investigate the role of G. duodenalis MIF (GdMIF) in activating the CD74-NF-κB-NLRP3 inflammasome pathway.
  • To determine the impact of GdMIF-induced inflammasome activation on intestinal damage during giardiasis.
  • To explore GdMIF's interaction with host cell receptors and its downstream effects.

Main Methods:

  • In vitro and in vivo studies using recombinant GdMIF (rGdMIF) and G. duodenalis-infected gerbils.
  • Investigated activation of NF-κB and NLRP3 inflammasome, GSDMD processing, and cytokine release.
  • Validated GdMIF interaction with CD74 using Co-immunoprecipitation (Co-IP) and Bimolecular Fluorescence Complementation (BiFC).
  • Utilized gene knockdown techniques (CD74, NF-κB) and a GdMIF blocking antibody.

Main Results:

  • GdMIF is an exocrine protein with dopamine tautomerase activity.
  • GdMIF activated NF-κB and NLRP3 inflammasome, leading to pyroptosis (GSDMD processing, LDH, and cytokine release).
  • GdMIF directly interacted with the CD74 receptor.
  • Knockdown of CD74 or NF-κB suppressed rGdMIF-induced inflammasome activation and cytokine production.
  • GdMIF blocking antibody reduced NLRP3 expression and intestinal damage in infected gerbils.
  • NLRP3 inhibition alleviated G. duodenalis-induced intestinal damage.

Conclusions:

  • GdMIF induces NLRP3 inflammasome activation and pyroptosis through CD74 receptor interaction.
  • This interaction triggers pro-inflammatory responses, contributing to intestinal damage in giardiasis.
  • Targeting the GdMIF-CD74-NLRP3 axis presents a potential therapeutic strategy for giardiasis.

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