This is pretty interesting right here. This could go in both directions.
To play their part in regulating their hosts’ immune systems, the bacteria in the microbiome fine-tune the levels of a protein responsible for the conversion of vitamin A to its active form in their hosts’ gastrointestinal tract, the researchers found.
Vaishnava’s team found that Firmicutes bacteria, particularly members of the class Clostridia, reduce the expression of a protein within the cells that line the intestines. The protein, retinol dehydrogenase 7 (Rdh7) converts dietary vitamin A to its active form, retinoic acid, Vaishnava says. The Clostridia bacteria, common to both mice and people, also promote increased vitamin A storage in the liver, the team found.
They will also explore the impacts of increased vitamin A storage in the liver due to bacteria Rdh7 regulation.
The other side,
# Downregulation of Th17 Cells in the Small Intestine by Disruption of Gut Flora in the Absence of Retinoic Acid
Th17 cells could be a big deal.
The results strongly suggest that RA deficiency altered gut microbiome, which in turn inhibited Th17 differentiation in the small intestine lamina propria.
Intestinal mucosa has a unique and complicated immune system composed of a variety of cell populations (1, 2). Among these, Th17 cells producing IL-17, IL-21, and IL-22 control immunity, inflammation, and infection at mucosal surfaces (3, 4). The lamina propria (LP) of the small and large intestines at steady state contains large numbers of IL-17–secreting Th17 cells and may thus influence intestinal homeostasis (3). Recent studies demonstrated preferential loss of Th17 cells in the gastrointestinal tract of HIV-infected patients (5, 6). In addition, IL-17 is required for host defense against oral Candida albicans , Staphylococcus aureus , and Citrobacter rodentium infection (7, 8). In the T cell-mediated colitis model, the recipient mice provoke disease by inducing IFN-γ and IL-17 secretion dependent on IL-23 production (9, 10). Other studies have shown that the adoptive transfer of IL-17–deficient cells results in a more aggressive colitis in the CD45RBhigh transfer model, which means that IL-17 plays a protective function in intestinal damages (11).