Abstract
Altered gut microbiota has been identified during psychological stress, which causes severe health issues worldwide. The integrity of the intestinal barrier and blood–brain barrier regulates the process of bacterial translocation and can supply the nervous system with real-time information about the environment. However, the association of gut microbiota with psychological stress remains to be fully interpreted. In this study, we established a psychological stress model using an improved communication box and compared the expression of tight junction proteins in multiple regions of the intestinal (duodenum, jejunum, ileum) and blood–brain (amygdala, hippocampus) barriers between model and control rats. We also conducted fecal microbiota analysis using 16S rRNA gene sequencing. Expression levels of the stress-related indicators adrenocorticotropic hormone, NR3C1,2, and norepinephrine were increased in the model group compared to control group. Psychological stress reduced brain and intestinal levels of tight junction proteins, including claudin5, occludin, α-actin, and ZO-1. Microbiota analysis revealed elevated microbial diversity and fecal proportions of Intestinimonas, Catenisphaera, and Globicatella in the model group. Further analysis indicated a negative correlation of Allisonella and Odoribacter, as well as a positive correlation of norank_f__Peptococcaceae, Clostridium_sensu_stricto_1, and Coprococcus_2, with claudin5, occludin, α-actin, and ZO-1. Our use of a rodent model to explore the association between compromised intestinal and blood–brain barriers and altered fecal microbiota under psychological stress improves our understanding of the gut–brain axis. Here, cues converge to control basic developmental processes in the intestine and brain such as barrier function. This study provides new directions for investigating the pathogenesis of emotional disorders and the formulation of clinical treatment.
Highlights
Stressful life events play an important role in the occurrence of mental illness; the unclear pathogenesis leads to many obstacles when forming a treatment plan (Goyal et al, 2014)
Another ten (n = 5, each group) rats were perfused with polyformaldehyde for rapid intestine and brain extraction. (iii) Brains were immersed in polyformaldehyde fixative and cut into parts to observe the expression of NR3C1 and NR3C2 in the cortex by immunohistochemistry. (iv) The remaining brain parts and intestines were immersed in polyformaldehyde fixative to observe the expression of claudin5, occludin, α-actin, and ZO-1 by immunohistochemistry, and to observe the structure of tight junctions by electron microscopy
The presence of the neurotransmitter NE in the brain is an essential indicator of psychological stress, and our results showed that psychological stress elevated NE levels in different brain areas of model rats compared to rats in the control group, as measured by High-performance liquid chromatography (HPLC)
Summary
Stressful life events play an important role in the occurrence of mental illness; the unclear pathogenesis leads to many obstacles when forming a treatment plan (Goyal et al, 2014). Repeated exposure to social stress can alter the diversity and composition of gut microbiota, accompanied by changes in microbial metabolites, cytokines, chemokines, and monoamine transmitters, which regulate behavior by stimulating the peripheral and central nervous systems (Braniste et al, 2014; Stilling et al, 2016). When these two essential barriers are damaged, short-chain fatty acids, lipopolysaccharide, and IL-6 can pass through the intestinal epithelium and increase their circulatory concentrations (Frost et al, 2014; Zuo et al, 2019). There are no systematic reports illustrating the effects of psychological stress on different tight junction proteins and regions of the intestinal barrier and BBB; different regions are associated with different functions and physiological environments
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