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Article

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

1
Department of Medicine, Augusta University, Augusta, GA 30912, USA
2
Department of Cell Biology and Anatomy, Augusta University, Augusta, GA 30912, USA
3
Department of Pediatrics, College of Medicine, University of Arkansas for Medical Sciences (UAMS), Little Rock, AR 72202, USA
4
Arkansas Children Nutrition Center, Arkansas Children’s Research Institute, Little Rock, AR 72202, USA
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Department of Infectious Diseases and Immunology, University of Florida, Gainesville, FL 32608, USA
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Georgia Cancer Center, Augusta University, Augusta, GA 30902, USA
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Department of Pathology, University of Notre Dame, Notre Dame, IN 46556, USA
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Institute of Healthy Aging, Augusta University, Augusta, GA 30912, USA
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Department of Pathology, Medical University of South Carolina, Charleston, SC 29403, USA
10
Ralph H Johnson Veterans Affairs Medical Center, Charleston, SC 29403, USA
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Burkhard Poeggeler
Int. J. Mol. Sci. 2021, 22(9), 5005; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22095005
Received: 7 April 2021 / Revised: 28 April 2021 / Accepted: 3 May 2021 / Published: 8 May 2021
(This article belongs to the Special Issue Tryptophan in Nutrition and Health)
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, Acetatifactor genus, Lachnospiraceae family, Enterococcus faecalis species, Clostridium sp genus, and Oscillibacter 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. View Full-Text
Keywords: tryptophan; systemic inflammation; dysbiosis; gut; microbiota tryptophan; systemic inflammation; dysbiosis; gut; microbiota
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MDPI and ACS Style

Yusufu, I.; Ding, K.; Smith, K.; Wankhade, U.D.; Sahay, B.; Patterson, G.T.; Pacholczyk, R.; Adusumilli, S.; Hamrick, M.W.; Hill, W.D.; Isales, C.M.; Fulzele, S. A Tryptophan-Deficient Diet Induces Gut Microbiota Dysbiosis and Increases Systemic Inflammation in Aged Mice. Int. J. Mol. Sci. 2021, 22, 5005. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22095005

AMA Style

Yusufu I, Ding K, Smith K, Wankhade UD, Sahay B, Patterson GT, Pacholczyk R, Adusumilli S, Hamrick MW, Hill WD, Isales CM, Fulzele S. A Tryptophan-Deficient Diet Induces Gut Microbiota Dysbiosis and Increases Systemic Inflammation in Aged Mice. International Journal of Molecular Sciences. 2021; 22(9):5005. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22095005

Chicago/Turabian Style

Yusufu, Ibrahim, Kehong Ding, Kathryn Smith, Umesh D. Wankhade, Bikash Sahay, G. T. Patterson, Rafal Pacholczyk, Satish Adusumilli, Mark W. Hamrick, William D. Hill, Carlos M. Isales, and Sadanand Fulzele. 2021. "A Tryptophan-Deficient Diet Induces Gut Microbiota Dysbiosis and Increases Systemic Inflammation in Aged Mice" International Journal of Molecular Sciences 22, no. 9: 5005. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22095005

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