Title :

Aluminum Ingestion Promotes Colorectal Hypersensitivity in Rodents.

Author(s) :

Esquerre, Nicolas [Auteur]
Basso, Lilian [Auteur]
Dubuquoy, Caroline [Auteur]
Djouina, Madjid [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Chappard, Daniel [Auteur]
Blanpied, Catherine [Auteur]
Desreumaux, Pierre [Auteur]
Vergnolle, Nathalie [Auteur]
Vignal, Cecile [Auteur]
Centre Lillois d’Études et de Recherches Sociologiques et Économiques - UMR 8019 [CLERSÉ]
Body-Malapel, Mathilde [Auteur]

Journal title :

Cellular and Molecular Gastroenterology and Hepatology

Abbreviated title :

Cell Mol Gastroenterol Hepatol

Volume number :

7

Pages :

185-196

Publication date :

2018-09-20

ISSN :

2352-345X

English keyword(s) :

Administration
Oral
Aluminum
Animals
Colon
Female
Hypersensitivity
Inflammation
Male
Mast Cells
Mice
Inbred C57BL
Mice
Knockout
Nociception
Rats
Sprague-Dawley
Receptor
PAR-2
Rectum
Visceral Pain
AlCi
aluminum citrate
CRD
colorectal distension
IBS
irritable bowel syndrome
IHC
immunohistochemistry
KO
knockout
MGG
May-Grünwald Giemsa
MPO
myeloperoxidase
Mast Cells
PAR
proteinase-activated receptor
PAR2
PCR
polymerase chain reaction
Risk Factors
Visceral Hypersensitivity
WT
wild-type
ZnCi
zinc citrate
mRNA
messenger RNA

English abstract : [en]

Irritable bowel syndrome (IBS) is a multifactorial disease arising from a complex interplay between genetic predisposition and environmental influences. To date, environmental triggers are not well known. Aluminum is ...
Show more >Irritable bowel syndrome (IBS) is a multifactorial disease arising from a complex interplay between genetic predisposition and environmental influences. To date, environmental triggers are not well known. Aluminum is commonly present in food, notably by its use as food additive. We investigated the effects of aluminum ingestion in rodent models of visceral hypersensitivity, and the mechanisms involved. Visceral hypersensitivity was recorded by colorectal distension in rats administered with oral low doses of aluminum. Inflammation was analyzed in the colon of aluminum-treated rats by quantitative PCR for cytokine expression and by immunohistochemistry for immune cells quantification. Involvement of mast cells in the aluminum-induced hypersensitivity was determined by cromoglycate administration of rats and in mast cell-deficient mice (Kit). Proteinase-activated receptor-2 (PAR2) activation in response to aluminum was evaluated and its implication in aluminum-induced hypersensitivity was assessed in PAR2 knockout mice. Orally administered low-dose aluminum induced visceral hypersensitivity in rats and mice. Visceral pain induced by aluminum persisted over time even after cessation of treatment, reappeared and was amplified when treatment resumed. As observed in humans, female animals were more sensitive than males. Major mediators of nociception were up-regulated in the colon by aluminum. Activation of mast cells and PAR2 were required for aluminum-induced hypersensitivity. These findings indicate that oral exposure to aluminum at human dietary level reproduces clinical and molecular features of IBS, highlighting a new pathway of prevention and treatment of visceral pain in some susceptible patients.Show less >

Audience :

Non spécifiée

Collections :

• Institut de Recherche Translationnelle sur l'Inflammation (INFINITE) - U1286

Research team(s) :

IBD and environnemental factors : epidemiology and functional analyses

Submission date :

2019-05-20T15:01:00Z
2019-05-20T15:15:01Z
2019-05-20T15:15:14Z