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Solute Transporter OCTN1/Slc22a4 Affects Disease Severity and Response to Infliximab in Experimental Colitis: Role of

Federica Del Chierico1, Letizia Masi2, Valentina Petito2

  • 1Immunology, Rheumatology and Infectious Diseases Research Area, Unit of Human Microbiome, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.

Inflammatory Bowel Diseases
|June 30, 2024
PubMed
Abstract

Insights

Genetic variations in the organic cation transporter 1 (OCTN1) influence gut microbiota and immune responses in inflammatory bowel diseases. OCTN1 deficiency in mice showed altered microbiota and immune cell profiles, impacting colitis severity and infliximab treatment efficacy.

Area of Science:

  • Gastroenterology
  • Immunology
  • Microbiology

Background:

  • Inflammatory bowel diseases (IBD) have complex, multifactorial origins.
  • Organic cation transporter 1 (OCTN1) may modulate inflammatory responses.
  • Genetic polymorphisms in OCTN1 are linked to increased IBD risk.

Purpose of the Study:

  • To investigate OCTN1's role in altering gut microbiota and mucosal immunity.
  • To assess OCTN1's impact on infliximab therapy response in a murine colitis model.

Main Methods:

  • Dextran sodium sulfate-induced colitis model in OCTN1 gene knockout and wild-type mice.
  • Intravenous infliximab administration to assess clinical efficacy.
  • Analysis of gut microbiota, histology, and T cell populations from stool, colon, and lymph node samples.

Main Results:

  • OCTN1 deficiency (Octn1-/-) altered microbiota profiles, worsening colitis-associated dysbiosis.
  • Infliximab treatment improved dysbiosis in both knockout and wild-type mice.
  • Octn1-/- mice exhibited milder disease and increased baseline Treg, Tmemory, Th2, and Th17 cells.

Conclusions:

  • The murine model supports studying OCTN1's genetic contribution to IBD.
  • OCTN1 may serve as a biomarker for inflammatory conditions.
  • OCTN1 could predict patient response to therapies.
Keywords:
OCTN1dextran sodium sulphate colitisgut microbiota

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