Back to Search
Start Over
Paneth cell defects induce microbiota dysbiosis In mice and promote visceral hypersensitivity
- Source :
- Gastroenterology, Gastroenterology, WB Saunders, 2017, in press, ⟨10.1053/j.gastro.2017.08.044⟩, Gastroenterology, WB Saunders, 2017, 153, pp.1594-1606. ⟨10.1053/j.gastro.2017.08.044⟩, Gastroenterology 6 (153), 1594-1606. (2017)
- Publication Year :
- 2017
- Publisher :
- HAL CCSD, 2017.
-
Abstract
- Background & Aims Separation of newborn rats from their mothers induces visceral hypersensitivity and impaired epithelial secretory cell lineages when they are adults. Little is known about the mechanisms by which maternal separation causes visceral hypersensitivity or its relationship with defects in epithelial secretory cell lineages. Methods We performed studies with C3H/HeN mice separated from their mothers as newborns and mice genetically engineered (Sox9 flox/flox -vil-cre on C57BL/6 background) to have deficiencies in Paneth cells. Paneth cells deficiency was assessed by lysozyme staining of ileum tissues and lysozyme activity in fecal samples. When mice were 50 days old, their abdominal response to colorectal distension was assessed by electromyography. Fecal samples were collected and microbiota were analyzed using GULDA quantitative PCR. Results Mice with maternal separation developed visceral hypersensitivity and defects in Paneth cells, as reported from rats, compared to mice without maternal separation. Sox9 flox/flox -vil-Cre mice also had increased visceral hypersensitivity compared to control littermate Sox9 flox/flox mice. Fecal samples from mice with maternal separation and from Sox9 flox/flox -vil-cre mice had evidence for intestinal dysbiosis of the microbiota, characterized by expansion of Escherichia coli . Daily gavage of conventional C3H/HeN adult mice with 10 9 commensal E. coli induced visceral hypersensitivity. Conversely, daily oral administration of lysozyme prevented expansion of E. coli during maternal separation and visceral hypersensitivity. Conclusions Mice with defects in Paneth cells (induced by maternal separation or genetically engineered) have intestinal expansion of E. coli leading to visceral hypersensitivity. These findings provide evidence that Paneth cell function and intestinal dysbiosis are involved in visceral sensitivity.
- Subjects :
- 0301 basic medicine
[SDV]Life Sciences [q-bio]
medicine.disease_cause
chemistry.chemical_compound
Feces
stress
0302 clinical medicine
Anxiety, Separation
lysozyme
Mice, Knockout
Mice, Inbred C3H
Gastroenterology
Age Factors
SOX9 Transcription Factor
Visceral Pain
3. Good health
medicine.anatomical_structure
Real-time polymerase chain reaction
Phenotype
Hyperalgesia
030211 gastroenterology & hepatology
Female
Lysozyme
Paneth Cells
Ileum
antimicrobial activity
abdominal pain
SOX9
Biology
03 medical and health sciences
FLOX
medicine
Escherichia coli
Animals
Genetic Predisposition to Disease
Hepatology
medicine.disease
Gastrointestinal Microbiome
Mice, Inbred C57BL
Disease Models, Animal
030104 developmental biology
chemistry
Animals, Newborn
Paneth cell
Immunology
Dysbiosis
Muramidase
Subjects
Details
- Language :
- English
- ISSN :
- 00165085
- Database :
- OpenAIRE
- Journal :
- Gastroenterology, Gastroenterology, WB Saunders, 2017, in press, ⟨10.1053/j.gastro.2017.08.044⟩, Gastroenterology, WB Saunders, 2017, 153, pp.1594-1606. ⟨10.1053/j.gastro.2017.08.044⟩, Gastroenterology 6 (153), 1594-1606. (2017)
- Accession number :
- edsair.doi.dedup.....5a0615c12818fffcb62e05916efcef43