Andrew van Kessel, Saskatchewan University, Canada, spoke about the link between nutrition, microflora and the host at the Lesaffre symposium held in Lille, France, November 8-9.

According to van Kessel, the abundant and taxonomically diverse microbial community colonizing the pig gastrointestinal tract evolves due to environmental and feed factors. Because each of the species of organisms in the intestine possess different capabilities and needs, the relative proportion of different species change in response to a variety of factors including age, diet composition, rearing environment and possibly genotype. Chemical composition of the diet is a major determinant of microbial composition since dietary nutriments are a major substrate for microbial fermentation. Changes in feed chemistry (ingredient selection) not only affect the species that will be advantaged, but also the type and abundance of fermentation products. Both composition and species changes are likely to be important in gut health and nutrition through direct competitive exclusion of pathogens, recognition by host receptors altering the gene expression as substrates for host metabolic pathways, or as toxins.

Butyrate, for example, has been identified as an energy source for colonocytes, an anti-inflammatory factor and an inhibitor of virulence genes in Salmonella. In contrast, ammonia is a colonocyte toxin, which might damage the epithelium increasing host susceptibility to disease.


Recently, van Kessel focused on the interactions of fiber and low quality protein associated with by-products use in pigs. High levels of non-digested protein from lower quality feed sources is available for fermentation as an energy source in the distal gut. There, it favors putrefactive bacterial species and yielding protein fermentation products. Dietary fiber can displace protein fermentation as an energy source in favor of protein utilization for microbial biomass synthesis (microbial protein, nucleic acid), reducing liberation of putative toxins. Using heat-treated soybean meal as a model protein, he observed increased concentrations of protein fermentation products in the colon, which were reduced by the addition of dietary fiber (sugar beet pulp, wheat bran).

High fermentable protein diets were associated with increased in markers of colon inflammation (cell turnover, mucin, pro-inflammatory cytokine expression) but limited changes in epithelial permeability. Interestingly, although fiber reduced several protein fermentation products, there was no amelioration of inflammatory response, suggesting as yet unidentified fermentation products or other factors mediated inflammation. Whether the responses lead to disease susceptibility and whether different fiber sources or feed additives (e.g. probiotics) can negate these outcomes will be subject to further investigation.