A Tryptophan-Deficient Diet Induces Gut Microbiota Dysbiosis and Increases Systemic Inflammation in Aged Mice

• Main Authors: Ibrahim Yusufu, Kehong Ding, Kathryn Smith, Umesh D. Wankhade, Bikash Sahay, G. Taylor Patterson, Rafal Pacholczyk, Satish Adusumilli, Mark W. Hamrick, William D. Hill, Carlos M. Isales, Sadanand Fulzele
• Format: Article
• Language: English
• Published: MDPI AG 2021-05-01
• Series: International Journal of Molecular Sciences
• Subjects: tryptophan; systemic inflammation; dysbiosis; gut; microbiota
• Online Access: https://www.mdpi.com/1422-0067/22/9/5005
• ISSN: 1661-6596; 1422-0067

The gut microflora is a vital component of the gastrointestinal (GI) system that regulates local and systemic immunity, inflammatory response, the digestive system, and overall health. Older people commonly suffer from inadequate nutrition or poor diets, which could potentially alter the gut microbiota. The essential amino acid (AA) tryptophan (TRP) is a vital diet component that plays a critical role in physiological stress responses, neuropsychiatric health, oxidative systems, inflammatory responses, and GI health. The present study investigates the relationship between varied TRP diets, the gut microbiome, and inflammatory responses in an aged mouse model. We fed aged mice either a TRP-deficient (0.1%), TRP-recommended (0.2%), or high-TRP (1.25%) diet for eight weeks and observed changes in the gut bacterial environment and the inflammatory responses via cytokine analysis (IL-1a, IL-6, IL-17A, and IL-27). The mice on the TRP-deficient diets showed changes in their bacterial abundance of Coriobacteriia class, <i>Acetatifactor</i> genus, Lachnospiraceae family, <i>Enterococcus faecalis</i> species, <i>Clostridium</i> sp genus, and <i>Oscillibacter</i> genus. Further, these mice showed significant increases in IL-6, IL-17A, and IL-1a and decreased IL-27 levels. These data suggest a direct association between dietary TRP content, the gut microbiota microenvironment, and inflammatory responses in aged mice models.