There is a growing appreciation for the specific
health benefits conferred by commensal microbiota
on their hosts. Clinical microbiota analysis and
animal studies in germ-free or antibiotic-treated mice
have been crucial for improving our understanding of
the role of the microbiome on the host mucosal
surface; however, studies on the mechanisms
involved in microbiome-host interactions remain
limited to small animal models. Here, we
demonstrated that rhesus monkeys under short-term
broad-spectrum antibiotic treatment could be used
as a model to study the gut mucosal host-microbiome
niche and immune balance with steady
health status. Results showed that the diversity and
community structure of the gut commensal bacteria
in rhesus monkeys were both disrupted after
antibiotic treatment. Furthermore, the 16S rDNA
amplicon sequencing results indicated that
Escherichia
-
Shigella
were predominant in stool
samples 9 d of treatment, and the abundances of
bacterial functional genes and predicted KEGG
pathways were significantly changed. In addition to
inducing aberrant morphology of small intestinal villi,
the depletion of gut commensal bacteria led to
increased proportions of CD3
+ T, CD4
+ T, and CD16
+
NK cells in peripheral blood mononuclear cells
(PBMCs), but decreased numbers of Treg and
CD20
+ B cells. The transcriptome of PBMCs from
antibiotic-treated monkeys showed that the immune
balance was affected by modulation of the
expression of many functional genes, including IL-13, VCAM1, and LGR4.
