High-protein diet differently modifies intestinal goblet cell characteristics and mucosal cytokine expression in ileum and colon

Lan, Annaïg; Andriamihaja, Mireille; Blouin, Jean-Marc; Liu, Xinxin; Descatoire, Véronique; Maredsous, Caroline Desclée de; Davila, Anne‐Marie; Walker, Francine; Tomé, Daniel; Blachier, François

doi:10.1016/j.jnutbio.2014.09.007

Cited by 49 publications

(43 citation statements)

References 31 publications

(37 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The sections were dehydrated with an alcohol concentration gradient (75%, 85%, 95%, and then 100%), cleared of alcohol with xylene, and sealed with neutral gum. Image-Pro Plus v. 6.0 (Media Cybernetics Inc., USA) was used to evaluate the goblet cells per unit area in the colonic mucosa [65].…”

Section: Morphological Observationsmentioning

confidence: 99%

Heat stress induced gut microbiota changes activate TLR4 / NF-κB signaling pathway contributing to inflammatory bowel disease in pigs

Hu¹,

Patil²,

Gong³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background Various stressors alter the 'brain-gut axis' and contribute to many gastrointestinal disorders such as inflammatory bowel disease. However, the pathological mechanisms of these perturbations are poorly understood. Here, we report on the induction of intestinal inflammation in heat-stressed pigs and apply fecal microbiota transplantation from pigs to mice to elucidate the role of intestinal microbiota in TLR4/NF-κB signaling pathway activation. Results Twelve healthy adult pigs were subjected to heat stress (34 ± 1 °C and 75–85% relative humidity) and compared with 12 control pigs exposed to 25 ± 3 °C and the same humidity level. The pigs were sacrificed on days 1, 7, 14, and 21. Their colonic contents were collected for microbiome analyses and their colonic epithelia underwent transcriptome analyses. Pseudo-germ-free mice were gavaged with fecal bacteria from heat-stressed and control pigs on the collection days to determine whether gut microbiomes and immune responses resembling those in the pigs could be induced in the mice. Heat-stressed pigs presented with fever and diarrhea from day 7 and their colonic villus length, crypt depth/width, and goblet cell number were significantly lower than those of the controls. Their TLR4, TRAF6, and nuclear p65 were upregulated at the RNA and protein levels. Their proinflammatory IL-6, IL-8, and IL-17 were also upregulated. Colonic microflora composition in the heat-stressed pigs markedly differed from that of the controls. By day 14, the former presented with substantial increases in opportunistic pathogens such as Campylobacterales , Veillonellaceae , and Megasphaera . Intestinal lipopolysaccharide concentrations were higher in the heat-stressed than the control pigs. Mice administered fecal transplantation from heat-stressed pigs had a distinctly different colonic microflora composition from those receiving control pig fecal transplantation. Bacteroides were significantly diminished and Akkermansia were significantly augmented in mice administered feces from heat-stressed pigs for 14 d. In the colonic tissues of mice given feces from heat-stressed pigs, the TLR4/NF-κB signaling pathway was activated and there was a mild inflammatory response. Conclusion Heat stress promotes changes in gut microflora composition which, in turn, activates the TLR4/NF-κB signaling pathway and causes inflammatory bowel disease in pigs.

show abstract

Section: Morphological Observationsmentioning

confidence: 99%

Heat stress induced gut microbiota changes activate TLR4 / NF-κB signaling pathway contributing to inflammatory bowel disease in pigs

Hu¹,

Patil²,

Gong³

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…Concerning the protective layer of mucus, which covers the intestinal epithelium but which is defective in IBD [38,39], several studies reported that an HP diet increases mucin gene expression in the small and large intestine epithelia of rats and pigs [37,40], probably as a result of an adaptive process towards the modified luminal environment [36]. Interestingly, a study in rats found different effects of an HP intake on the mucus layer according to the protein source [41].…”

Section: Potential Influence Of Dietary Proteins On Inflammatory Bmentioning

confidence: 99%

“…In addition, conflicting results have been obtained on the effects of an HP diet on intestinal immunity. In rats, the HP diet decreased myeloperoxidase activity, toll-like receptor 4, and cytokine gene expression in the ileum, while it virtually did not affect these parameters in the colon [40]. In pigs fed an HP diet, both pro- and anti-inflammatory gene expressions were found to be increased in the colonic mucosa [37].…”

Section: Potential Influence Of Dietary Proteins On Inflammatory Bmentioning

confidence: 99%

Dietary Protein and Amino Acid Supplementation in Inflammatory Bowel Disease Course: What Impact on the Colonic Mucosa?

et al. 2017

Self Cite

View full text Add to dashboard Cite

Inflammatory bowel diseases (IBD), after disease onset, typically progress in two cyclically repeated phases, namely inflammatory flare and remission, with possible nutritional status impairment. Some evidence, either from epidemiological, clinical, and experimental studies indicate that the quantity and the quality of dietary protein consumption and amino acid supplementation may differently influence the IBD course according to the disease phases. For instance, although the dietary protein needs for mucosal healing after an inflammatory episode remain undetermined, there is evidence that amino acids derived from dietary proteins display beneficial effects on this process, serving as building blocks for macromolecule synthesis in the wounded mucosal area, energy substrates, and/or precursors of bioactive metabolites. However, an excessive amount of dietary proteins may result in an increased intestinal production of potentially deleterious bacterial metabolites. This could possibly affect epithelial repair as several of these bacterial metabolites are known to inhibit colonic epithelial cell respiration, cell proliferation, and/or to affect barrier function. In this review, we present the available evidence about the impact of the amount of dietary proteins and supplementary amino acids on IBD onset and progression, with a focus on the effects reported in the colon.

show abstract

“…Other studies also demonstrate that increased dietary protein correlates with increased ammonia production and other putrefactive products in the colon (Gibson et al, 1976; Macfarlane et al, 1986; Richardson et al, 2013). Increased putrefaction in the distal gut increases putrefactive metabolite production, which can be toxic to colonocytes (Cummings et al, 1979) and can induce inflammation (Lan et al, 2015). Indeed, prospective human and animal studies demonstrate that excess protein in the diet can lead to damage in the colon (increased relapse risk in ulcerative colitis in humans (Jowett et al, 2004), increased colonic DNA damage and thinned colonic mucus barrier in rats, depending on protein type (Toden et al, 2007), reduced brush border membrane height in rats (Andriamihaja et al, 2010), decreased telomere length and increased DNA breaks in colonic cells of rats fed red meat, which were reversed with addition of resistant starch (Toden et al, 2007; Toden et al, 2007; O’Callaghan et al, 2012) and increased risk of post-weaning diarrhea in piglets (Heo et al, 2009; Kim et al, 2011)).…”

Section: Introductionmentioning

confidence: 99%

Personalizing protein nourishment

Dallas

Sanctuary

et al. 2017

Critical Reviews in Food Science and Nutrition

View full text Add to dashboard Cite

Proteins are not equally digestible—their proteolytic susceptibility varies by their source and processing method. Incomplete digestion increases colonic microbial protein fermentation (putrefaction), which produces toxic metabolites that can induce inflammation in vitro and have been associated with inflammation in vivo. Individual humans differ in protein digestive capacity based on phenotypes, particularly disease states. To avoid putrefaction-induced intestinal inflammation, protein sources and processing methods must be tailored to the consumer’s digestive capacity. This review explores how food processing techniques alter protein digestibility and examines how physiological conditions alter digestive capacity. Possible solutions to improving digestive function or matching low digestive capacity with more digestible protein sources are explored. Beyond the ileal digestibility measurements of protein digestibility, less invasive, quicker and cheaper techniques for monitoring the extent of protein digestion and fermentation are needed to personalize protein nourishment. Biomarkers of protein digestive capacity and efficiency can be identified with the toolsets of peptidomics, metabolomics, microbial sequencing and multiplexed protein analysis of fecal and urine samples. By monitoring individual protein digestive function, the protein component of diets can be tailored via protein source and processing selection to match individual needs to minimize colonic putrefaction and, thus, optimize gut health.

show abstract

High-protein diet differently modifies intestinal goblet cell characteristics and mucosal cytokine expression in ileum and colon

Cited by 49 publications

References 31 publications

Heat stress induced gut microbiota changes activate TLR4 / NF-κB signaling pathway contributing to inflammatory bowel disease in pigs

Heat stress induced gut microbiota changes activate TLR4 / NF-κB signaling pathway contributing to inflammatory bowel disease in pigs

Dietary Protein and Amino Acid Supplementation in Inflammatory Bowel Disease Course: What Impact on the Colonic Mucosa?

Personalizing protein nourishment

Contact Info

Product

Resources

About