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Review

Stress in the microbiome-immune crosstalk

Article: 2327409 | Received 17 Oct 2023, Accepted 04 Mar 2024, Published online: 15 Mar 2024

Figures & data

Figure 1. AI-2 system in E. coli and AHL system in gram negative bacteria.

In E. coli, AI-2 is produced by LuxS, while AHL in Gram negative bacteria is produced by LuxL. In E coli, AI-2 is sensed by LsrB, which captures AI-2 into the bacteria. AI-2 is then phosphorylated by LsrK. Phosphorylation triggers AI-2 degradation. AHLs, in contrast, bind to LuxR to modulate the expression of genes required for virulence, biofilm formation, etc.
Figure 1. AI-2 system in E. coli and AHL system in gram negative bacteria.

Figure 2. Effects of the microbiota on intestinal immune response.

Signals (QSM, bacteria, microbial metabolites, neurotransmitters, neuropeptides) originating from the microbiota affect the intestinal epithelial cells, enterochromaffin cells, or diffuse through the intestinal barrier, to modulate immune cells (T cells, dendritic cells, etc.) present in the lamina propria. Microbial signals and immune cells often reach the bloodstream and migrate to the brain. Here are presented cells relevant for the stress behavioral effects.
Figure 2. Effects of the microbiota on intestinal immune response.

Figure 3. Effects of stress on the microbiota and the immune response.

Stress hormones such as norepinephrine, epinephrine, and cortisol, impact the microbiota diversity and metabolites. Associated with stress, there is an increase of cytokine production but a decrease in various populations of immune cells. The increase of proinflammatory cytokines leads to increased differentiation of Th17 cells.
Figure 3. Effects of stress on the microbiota and the immune response.