Blake C. Guard, MS, PhD
Gastrointestinal Laboratory, Department of Small Animal Clinical Sciences, Texas A&M University, College Station, TX, USA
Keynote Message
The intestinal microbiota affect host health through stimulation of the immune system, development of gut structure, and aiding in the defence against invading pathogens. Microbial metabolism helps to promote host health through the production of metabolic end products (e.g., short-chain fatty acids, secondary bile acids, vitamins). Inflammatory bowel disease (IBD), metabolic syndrome, cancer, asthma, diabetes, obesity, and stress-related disorders are examples of human diseases where the microbiota have been implicated. Chronic diarrhoea in dogs is thought to be a multifactorial disease which can involve genetic predisposition, improper activation of the immune system, dietary sensitivities, and microbial dysbiosis. Recently, alterations in faecal bile acids have been noted in human patients with IBD. Preliminary studies in dogs with chronic diarrhoea suggest that faecal bile acids in dogs are altered. During this session, microbial dysbiosis, metabolomics, and faecal bile acid dysmetabolism in healthy dogs and dogs with chronic diarrhoea will be described. Furthermore, methods for altering bile acid dysmetabolism in dogs will be discussed.
Key References
1. Guard BC, Barr JW, Reddivari L, Klemashevich C, Jayaraman A, Steiner JM, Vanamala J, Suchodolski JS. Characterization of microbial dysbiosis and metabolomic changes in dogs with acute diarrhea. PLoS One. 2015;10(5):e0127259. DOI: 10.1371/journal.pone.0127259.
2. Guard BC, Suchodolski JS. Horse species symposium: Canine intestinal microbiology and metagenomics: From phylogeny to function. Journal of Animal Science. 2016;94(6):2247–61. DOI: 10.2527/jas.2015-0029.
3. Guard BC, Honneffer JB, Jonika MM, Lidbury JA, Steiner JM, Jergens A, Suchodolski JS. Longitudinal characterization of dysbiosis and unconjugated bile acid profiles in the feces of dogs with inflammatory bowel disease. Gastroenterology. 2017;152(5):S992. DOI: 10.1016/S0016-5085(17)33361-9.