Dietary Protein and Fiber Affect Gut Microbiome and Treg/Th17 Commitment in Chronic Kidney Disease Mice.
Am J Nephrol
; 53(8-9): 646-651, 2022.
Article
em En
| MEDLINE
| ID: mdl-36349783
ABSTRACT
BACKGROUND:
Patients with chronic kidney disease (CKD) have dysbiosis, dysmetabolism, and immune dysregulation. Gut microbiome plays an important role shaping the immune system which is an important modulator of CKD progression.METHODS:
We compared the effect of a diet low in protein and high in fiber (LP-HF; n = 7) to that of diet rich in protein, but low in fiber (HP-LF; n = 7) on gut microbiome and T-cell commitment in male CKD (Alb/TGF-ß1) mice. The gut microbiomes of these mice were subjected to 16S rRNA taxonomic profiling at baseline, 6 weeks and 12 weeks of the study.RESULTS:
The LP-HF diet was associated with an increase in Butyricicoccus pullicaecorum BT, a taxon whose functions include those closely related to butyric acid synthesis (Kendall's W statistic = 180 in analysis of microbiome composition). HP-LF diet was associated with increased abundance of two predominantly proteolytic bacterial strains related to Parabacteroides distasonis (W statistic = 173), Mucispirillum schaedleri, and Bacteroides dorei (W statistic = 192). Pathway analysis suggested that the LP-HF diet induced carbohydrate, lipid, and butyrate metabolism. As compared with HP-LF mice, LP-HF mice had 1.7-fold increase in CD4+Foxp3+Treg cells in spleen and 2.4-fold increase of these cells in peripheral blood. There was an 87% decrease in percentage of CD4+ Th17 + cells in spleen and an 85% decrease in peripheral blood, respectively, in LP-HF mice compared to the HP-LF mice.CONCLUSION:
The LP-HF diet promotes the proliferation of saccharolytic bacteria and favors T-cell commitment toward Treg cells in a CKD mouse of model. Clinical significance of the finding needs to be further investigated.Palavras-chave
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Base de dados:
MEDLINE
Assunto principal:
Insuficiência Renal Crônica
/
Microbioma Gastrointestinal
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article