Dietary iron is necessary to support proliferative regeneration following intestinal injury.

intestinal injury intestinal proliferation iron tissue repair wound healing

Journal

The Journal of nutrition
ISSN: 1541-6100
Titre abrégé: J Nutr
Pays: United States
ID NLM: 0404243

Informations de publication

Date de publication:
19 Jan 2024
Historique:
received: 06 10 2023
revised: 04 12 2023
accepted: 04 01 2024
medline: 22 1 2024
pubmed: 22 1 2024
entrez: 21 1 2024
Statut: aheadofprint

Résumé

Tissue repair and regeneration in the gastrointestinal system is crucial for maintaining homeostasis, with the process relying on intricate cellular interactions and affected by micro and macro-nutrients. Iron, essential for various biological functions, plays a dual role in tissue healing by potentially causing oxidative damage and participating in anti-inflammatory mechanisms, underscoring its complex relationship with inflammation and tissue repair. The study aimed to elucidate the role of low dietary iron in gastrointestinal tissue repair. We utilized quantitative iron measurements to assess iron levels in inflamed regions of ulcerative colitis and Crohn's disease patients. Additionally, three mouse models of gastrointestinal injury/repair (dextran sulfate sodium-induced colitis, radiation injury, and wound biopsy) were used to assess the effects of low dietary iron on tissue repair. We found that levels of iron in inflamed regions of both ulcerative colitis and Crohn's disease patients are elevated. Similarly, during gastrointestinal repair, iron levels were found to be heightened, specifically in intestinal epithelial cells across the three injury/repair models. Mice on a low iron diet showed compromised tissue repair with reduced proliferation. In standard diet, epithelial cells and the stem cell compartment maintain adequate iron stores. However, during a period of iron deficiency, epithelial cells exhaust their iron reserves while the stem cell compartment maintain their iron pools. During injury, when the stem compartment in disrupted, low iron levels impair proliferation and compromise repair mechanisms. Low dietary iron impairs intestinal repair through compromising the ability of epithelial cells to aid in intestinal proliferation.

Sections du résumé

BACKGROUND BACKGROUND
Tissue repair and regeneration in the gastrointestinal system is crucial for maintaining homeostasis, with the process relying on intricate cellular interactions and affected by micro and macro-nutrients. Iron, essential for various biological functions, plays a dual role in tissue healing by potentially causing oxidative damage and participating in anti-inflammatory mechanisms, underscoring its complex relationship with inflammation and tissue repair.
OBJECTIVE OBJECTIVE
The study aimed to elucidate the role of low dietary iron in gastrointestinal tissue repair.
METHODS METHODS
We utilized quantitative iron measurements to assess iron levels in inflamed regions of ulcerative colitis and Crohn's disease patients. Additionally, three mouse models of gastrointestinal injury/repair (dextran sulfate sodium-induced colitis, radiation injury, and wound biopsy) were used to assess the effects of low dietary iron on tissue repair.
RESULTS RESULTS
We found that levels of iron in inflamed regions of both ulcerative colitis and Crohn's disease patients are elevated. Similarly, during gastrointestinal repair, iron levels were found to be heightened, specifically in intestinal epithelial cells across the three injury/repair models. Mice on a low iron diet showed compromised tissue repair with reduced proliferation. In standard diet, epithelial cells and the stem cell compartment maintain adequate iron stores. However, during a period of iron deficiency, epithelial cells exhaust their iron reserves while the stem cell compartment maintain their iron pools. During injury, when the stem compartment in disrupted, low iron levels impair proliferation and compromise repair mechanisms.
CONCLUSIONS CONCLUSIONS
Low dietary iron impairs intestinal repair through compromising the ability of epithelial cells to aid in intestinal proliferation.

Identifiants

DOI: 10.1016/j.tjnut.2024.01.013 PMID: 38246358
pubmed: 38246358
pii: S0022-3166(24)00032-4
doi: 10.1016/j.tjnut.2024.01.013
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 American Society for Nutrition. Published by Elsevier Inc. All rights reserved.

Auteurs

Wesley Huang (W)

Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA; Department of Cellular and Molecular Biology, University of Michigan, Ann Arbor, MI, USA; Medical Scientist Training Program, University of Michigan, Ann Arbor, MI, USA.

Nupur K Das (NK)

Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.

Megan D Radyk (MD)

Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.

Theresa Keeley (T)

Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.

Miguel Quiros (M)

Department of Biochemistry, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.

Chesta Jain (C)

Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.

Marwa O El-Derany (MO)

Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA; Department of Biochemistry, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.

Thaarini Swaminathan (T)

Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.

Sofia Dziechciarz (S)

Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.

Joel K Greenson (JK)

Department of Pathology, University of Michigan, Ann Arbor, MI, USA.

Asma Nusrat (A)

Department of Pathology, University of Michigan, Ann Arbor, MI, USA.

Linda C Samuelson (LC)

Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.

Yatrik M Shah (YM)

Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA; Department of Cellular and Molecular Biology, University of Michigan, Ann Arbor, MI, USA. Electronic address: shahy@umich.edu.

Classifications MeSH