Repository hosted by TU Delft Library

Home · Contact · About · Disclaimer ·
 

Lactobacillus plantarum NCIMB8826 ameliorates inflammation of colon and skin in human APOC1 transgenic mice

Publication files not online:

Author: Mariman, R. · Reefman, E. · Tielen, F. · Persoon-Deen, C. · Mark, K. van de · Worms, N. · Koning, F. · Nagelkerken, L.
Type:article
Date:2016
Source:Beneficial Microbes, 2, 7, 215-225
Identifier: 534559
doi: DOI:10.3920/BM2015.0074
Keywords: Biology · APOC1+/+ transgenic mice model · Gene expression profiling · Intestine · Mast cells · Probiotics · Biomedical Innovation · Healthy Living · Life · MHR - Metabolic Health Research · ELSS - Earth, Life and Social Sciences

Abstract

Genetic predisposition and environmental factors, including the gut microbiota, have been suggested as major factors in the development and progression of atopic dermatitis. Hyperlipidemic human APOC1+/+ transgenic mice display many features of human atopic dermatitis, such as scaling, lichenification, excoriations, and pruritus, along with a disturbed skin barrier function. Cytokine analysis of serum shows an increase of various pro-inflammatory cytokines, including interleukin (IL)-12p40, IL-6, and IL-1α, but lower levels of interferon-γ. These mice also display aspects of colitis evident from macroscopic and histological abnormalities. Genome-wide transcriptome analysis of the intestine shows up-regulation of several genes associated with mast cells and eosinophils and this observation was confirmed by demonstrating increased numbers of IgE+ and FcRε+ mast cells in the colon and in the skin. Oral treatment with Lactobacillus plantarum NCIMB8826 resulted in decreased numbers of mast cells in the colon. Moreover, this L. plantarum strain ameliorated skin pathology, evident from improved skin barrier integrity, absence of skin thickening, and less excoriations. These results suggest that modulation of intestinal immune homeostasis contributes to the suppression of atopic dermatitis. © 2015 Wageningen Academic Publishers.