The results presented here highlight that single microbial metabolite regulates the barrier function in epithelial cells via the activating AhR-Nrf2 signaling pathways and also anti-inflammatory activities in AhR dependent pathways.
Although these findings highlight the important role of microbial structures in regulating barrier function, another layer of complexity is the relationship between the bioactive potential of the microbiota and the intestinal barrier.
The imbalance in Pseudomonas species seen in our study might be a secondary consequence of defective mucosal barrier function and microbial killing present in IBD patients [50].
Oral epithelia function as a microbial barrier and are actively involved in recognizing and responding to bacteria.
These include regulation of intestinal microbial homeostasis, maintenance of the gastrointestinal barrier function, interference with the ability of pathogens to colonize [16], [17], [18], [19], [20], [21], [22] and finally modulation of local and systemic immune responses [23].
However, little is known about the role of these cells in HIV infection, a disease fuelled by intestinal inflammation, a loss of epithelial barrier function and increased microbial translocation (MT).
The human gastrointestinal tract contains bacterial species that, among other functions, maintain a microbial barrier against potential pathogens and help regulate the immune response in the human body.
Although the etiology of NEC is incompletely understood, contributing factors are thought to include immature intestinal motility and barrier function, inappropriate initial gut microbial colonization and perinatal hypoxia/ischemia [76].
Both alcohol consumption and HIV/SIV infection seem to disrupt the intestinal lining, disrupt intestinal barrier function, and lead to microbial translocation.
It is hypothesized that impaired intestinal barrier function enables organisms and microbial products to translocate from the gut to the mesenteric lymph nodes, liver, and systemic circulation [ 17– 19]; however, this is a difficult domain of the causal pathway to evaluate.
