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Related Experiment Video

Updated: Jun 9, 2026

The Citrobacter rodentium Mouse Model: Studying Pathogen and Host Contributions to Infectious Colitis
11:04

The Citrobacter rodentium Mouse Model: Studying Pathogen and Host Contributions to Infectious Colitis

Published on: February 19, 2013

ATPIF1 Deficiency Significantly Alleviates Citrobacter rodentium-Induced Colitis in Mice.

Haoyu Yang1,2, Ziqi Li1,2, Dong Yan2

  • 1College of Biological and Chemical Engineering, Changsha University, Changsha 410022, Hunan, P. R. China.

Journal of Microbiology and Biotechnology
|June 8, 2026
PubMed
Summary
This summary is machine-generated.

Mitochondrial ATP synthase inhibitory factor 1 (ATPIF1) deficiency protects against Citrobacter rodentium-induced colitis. ATPIF1 knockout mice showed reduced inflammation, improved gut barrier function, and stabilized gut microbiota, suggesting ATPIF1 as a therapeutic target.

Keywords:
Infection-associated colitisMicrobiotaMitochondrial ATPase inhibitory factor 1 (ATPIF1)NOD-like receptor protein 3 (NLRP3)

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4D Multimodality Imaging of Citrobacter rodentium Infections in Mice
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Published on: August 13, 2013

Area of Science:

  • Cellular biology
  • Immunology
  • Microbiology

Background:

  • Mitochondrial ATP synthase inhibitory factor 1 (ATPIF1) is involved in cellular energy metabolism and inflammation.
  • The specific role of ATPIF1 in infection-associated colitis is not well understood.

Purpose of the Study:

  • To investigate the impact of ATPIF1 on host susceptibility and inflammation during Citrobacter rodentium-induced infectious colitis.
  • To evaluate the protective effects of ATPIF1 deficiency in a mouse model of colitis.

Main Methods:

  • Utilized ATPIF1 knockout (KO) and wild-type (WT) mice challenged with Citrobacter rodentium.
  • Assessed disease severity (body weight, DAI, colon length), histopathology, barrier function (ZO-1), inflammatory markers (IL-1β, TNF-α, NLRP3 inflammasome), and gut microbiota (16S rRNA sequencing).

Main Results:

  • ATPIF1 deficiency significantly alleviated colitis symptoms, including reduced weight loss and colon shortening.
  • KO mice demonstrated preserved epithelial integrity, increased goblet cells, and enhanced barrier function (ZO-1 expression).
  • Reduced inflammatory cell infiltration, lower pro-inflammatory cytokine levels (IL-1β, TNF-α), and attenuated NLRP3 inflammasome activation were observed in KO mice. Gut microbiota composition was stabilized, with reduced pathogenic bacteria expansion.

Conclusions:

  • ATPIF1 deficiency confers a protective phenotype against C. rodentium-induced colitis.
  • This protection is associated with reduced inflammation, improved barrier function, enhanced pathogen clearance, and a more stable gut microbiota.
  • ATPIF1 emerges as a potential therapeutic target for managing infection-associated colitis.