The physiological consequences of stress often manifest in the gastrointestinal tract. Traumatic or chronic stress is associated with widespread maladaptive changes throughout the gut, although comparatively little is known about the effects of acute stress. Furthermore, these stress‐induced changes in the gut may increase susceptibility to gastrointestinal disorders and infection, and impact critical features of the neural and behavioural consequences of the stress response by impairing gut–brain axis communication. Understanding the mechanisms behind changes in enteric nervous system circuitry, visceral sensitivity, gut barrier function, permeability, and the gut microbiota following stress is an important research objective with pathophysiological implications in both neurogastroenterology and psychiatry. Moreover, the gut microbiota has emerged as a key aspect of physiology sensitive to the effects of stress. In this review, we focus on different aspects of the gastrointestinal tract including gut barrier function as well as the immune, humoral and neuronal elements involved in gut–brain communication. Furthermore, we discuss the evidence for a role of stress in gastrointestinal disorders. Existing gaps in the current literature are highlighted, and possible avenues for future research with an integrated physiological perspective have been suggested. A more complete understanding of the spatial and temporal dynamics of the integrated host and microbial response to different kinds of stressors in the gastrointestinal tract will enable full exploitation of the diagnostic and therapeutic potential in the fast‐evolving field of host–microbiome interactions.

The impact of acute and chronic stress on gastrointestinal physiology and function: a microbiota–gut–brain axis perspective

This article examines the involvement of the brain-derived neurotrophic factor (BDNF) in the control of nociception and pain. BDNF, a neurotrophin known for its essential role in neuronal survival and plasticity, has garnered significant attention for its potential implications as a modulator of synaptic transmission. This comprehensive review aims to provide insights into the multifaceted interactions between BDNF and pain pathways, encompassing both physiological and pathological pain conditions. I delve into the molecular mechanisms underlying BDNF’s involvement in pain processing and discuss potential therapeutic applications of BDNF and its mimetics in managing pain. Furthermore, I highlight recent advancements and challenges in translating BDNF-related research into clinical practice.

Brain-Derived Neurotrophic Factor, Nociception, and Pain

Irritable bowel syndrome (IBS) is a prevalent functional gastrointestinal disorder, however, its effect on gut microbiota during the periadolescent period remains unclear. In this study, our objective was to investigate the characteristics of gut microbiota in male periadolescent rats with IBS induced by neonatal maternal separation (NMS). We evaluated visceral sensitivity by electromyography (EMG), analyzed gut microbiota composition using 16S rDNA gene sequencing, and examined intestinal pathological changes between control and IBS-like groups. The IBS-like group had significantly higher discharge amplitude of the external oblique muscle of the abdomen during colorectal distension (CRD) at 40- and 60 mmHg pressures. We observed differences in gut microbiota composition, with an increase in Bacteroidetes abundance and a decrease in Firmicutes in IBS-like rats. Beta-diversity analysis revealed the gut microbiota of the IBS-like group displayed higher consistent, while that of the control group exhibited substantial variation. Linear discriminant analysis effect size (LEfSe) detected 10 bacterial taxonomic clades showing statistically significant differences (7 increased and 3 decreased) in the IBS-like group. Functional analysis revealed that aminoacyl-tRNA biosynthesis and fatty acid biosynthesis were significantly altered, leading to changes in gene expression. Our findings demonstrate a definite correlation between gut microbiota dysbiosis and IBS during the male periadolescent period, with Alloprevotella and Bacteroide positively associated with high risk of IBS. The effects of specific bacterial genera may provide new insights for the development of treatments for IBS. 

Characteristics of gut microbiota in male periadolescent rats with irritable bowel syndrome

Chronodisruption, commonly displayed by people living with obesity (PLO), is linked to colonic microbiota dysbiosis, and may increase the risk of many chronic non-communicable diseases, whereas dietary interventions–called chrononutrition may mitigate it. We evaluated the in vitro effects of spent coffee grounds (SCG), and their antioxidant dietary fiber (SCG-DF) on the colonic microbiota of an obese donor displaying dysbiosis and chronodisruption. Basal microbiota pattern was associated with an increased risk of non-communicable chronic diseases. Both samples decrease species richness and increase microbiota diversity (p < 0.05; Chao and Shannon index, respectively), positively enhancing Firmicutes/Bacteroidetes index (SCG, p < 0.04; SCG-DF, p < 0.02). SCG and SCG-DF modulated the microbiota, but SCG-DF induced greater changes, significantly increasing. p_Actonobacterias (SCG p < 0.04; SCG-DF, p < 0.02), and reducing g_Alistipes; s_putredinis, g_Prevotella;s_copri. The highest increase was displayed by p_Proteobacteria (f_Desulfovibrionaceae and f_Alcanigenaceae, p < 0.05), while g_Haemophilus; s_parainfluenzae decreased (p < 0.05). However, neither SCG nor SCG-DF modulated g_Alistipes (evening-type colonic microbial marker) beneficially. SCG and SCG-DF reduced (p < 0.05) g_Lachnospira, a microbial evening-type marker, among other microbial populations, of an obese donor displaying chronodisruption and dysbiosis. SCG and SCG-DF displayed a prebiotic effect with the potential to mitigate diseases linked to chronodisruption. 

Spent coffee grounds and its antioxidant dietary fiber promote different colonic microbiome signatures: Benefits for subjects with chronodisruption

Background Visceral hypersensitivity (VH) is one of the most common causes of irritable bowel syndrome (IBS). The anti-hyperalgesic effects of metabotropic glutamate receptor 8 (mGluR8) has been identified in the central nervous system (CNS). However, whether this receptor has a similar function in the gastrointestinal tract has not been well studied. The present study aimed to explore the role of this receptor in a visceral hypersensitivity-related IBS rat model. Methods Neonatal rats were separated from their mothers for 3 hours daily from postnatal day 2 to day 14 to establish neonatal maternal separation (NMS) models. The mGluR8 agonist (S)-3,4-DCPG (10 mg/kg) and the mGluR8 antagonist (RS)-α- methylserine-O-phosphate (MSOP) (10 mg/kg) were used to examine the role of mGLuR8 in the NMS rats. The expression of mGluR8, related inflammatory factors, and inflammatory signal pathways were assessed in colon tissues. Results Our data showed that mGluR8 expression was increased in the colonic mucosa of NMS rats compared to controls. In addition, selective activation of mGluR8 ameliorated visceral hypersensitivity, whereas antagonization of mGluR8 aggravated visceral hypersensitivity. Treatment with (S)-3,4-DCPG (10 mg/kg) reduced the expression of myeloperoxidase (MPO) in intestinal mucosa of NMS rats. Furthermore, activating mGluR8 reduced the expression of tumor necrosis factor-α (TNF-α), whereas antagonizing mGluR8 promoted that. The expressions of toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) did not significantly change upon activation or antagonization of mGluR8 receptor. Conclusions The activation of mGluR8 receptor ameliorates visceral hypersensitivity in NMS rats, and the underlying mechanisms may be associated with the inhibition of TNF-α and the suppression of colonic inflammatory response.

Metabotropic glutamate receptor-8 relieves neonatal maternal separation-induced visceral hypersensitivity in rats by regulating expression of TNF-α

Recent studies have demonstrated the vital role of P2X4 receptors (a family of ATP-gated non-selective cation channels) in the transmission of neuropathic and inflammatory pain. In this study, we investigated the role of spinal P2X4 receptors in chronic functional visceral hypersensitivity of neonatal maternal separation (NMS) rats. A rat model of irritable bowel syndrome was established by neonatal maternal separation. Visceral sensitivity was assessed by recording the response of the external oblique abdominal muscle to colorectal distension. P2X4 receptor antagonist and agonist were administrated intrathecally. The expression of P2X4 receptor was examined by Western Blot and immunofluorescence. The effect of P2X4 receptor antagonist on expression of brain-derived neurotrophic factor (BDNF) was assessed by Western Blot. We found neonatal maternal separation enhanced visceral hypersensitivity and increased the expression of P2X4 receptor in spinal thoracolumbar and lumbosacral segments of rats. Pharmacological results showed that visceral sensitivity was attenuated after intrathecal injection of P2X4 receptor antagonist, 5-BDBD, at doses of 10 nM or 100 nM, while visceral sensitivity was enhanced after intrathecal injection of P2X4 receptor agonist C5-TDS at doses of 10 μM or 15 μM. In addition, the spinal expression of BDNF significantly increased in NMS rats and intrathecal injection of 5-BDBD significantly decreased the expression of BDNF especially in NMS rats. C5-TDS failed to increase EMG amplitude in the presence of ANA-12 in control rats. Our results suggested the spinal P2X4 receptors played an important role in visceral hypersensitivity of NMS rats through BDNF. 

Spinal P2X4 Receptors Involved in Visceral Hypersensitivity of Neonatal Maternal Separation Rats

Yogurt consumption shows a wide range of effects on the gut microbial composition, and correlation of components in yogurt with the changes of gut microbia remains largely uncharacterized. We aimed to determine the effect of brown yogurt (SSN) on the composition of the gut microbiota and to explore the effects of the major components. We performed a randomized study of 70 healthy adults to compare the effects of SSN and standard probiotic-containing yogurt (YJD) during a 28-day intervention and a 10-day follow-up period. The results showed that the SSN group showed significant increases in the butyrate-producer Akkermansia muciniphila, Ruminococcus, and Veillonella (p < 0.05), whereas the YJD group showed increases in the butyrate-producer Megasphaera, Anaerostipes, and Eubacterium. There were reductions in the potential pathogens Haemophilus parainfluenzae and Gemmiger formicilis in both groups (p < 0.05). The SSN group had more Faecalibacterium prausnitzii, Prevotella copri, Bifidobacterium and B. longum than the YJD group (p < 0.001), but fewer Bacteroides, unspecified Clostridiales and Coprococcus eutactus (p < 0.01). These differences might be at least in part explained by the higher concentrations of monosaccharide, palmitoleic acid, and glutamine synthetase adenyltransferase in the SSN product (p < 0.05), which were positively associated with F. prausnitzii (p ≤ 0.001) and B. longum (p < 0.05), and negatively associated with C. eutactus (p < 0.01). The single strain of starter culture and lower content of polyunsaturated fatty acids (PUFA) in the SSN product were also related to the different changes of gut microbia, and the taxa F. prausnitzii, Bifidobacterium and B. longum were negatively associated with starter culture and PUFA (p < 0.01). These findings suggested that SSN is rich in prebiotic components and might be beneficial for healthy adults. Furthermore, bacterial taxa with potential health benefits could be encouraged through improving the formulation and technology used to produce the dairy products.

Changes in the intestinal microbiota of healthy adults induced by brown yogurt and relationships of bacterial taxa with specific components.

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Spinal P2X4 Receptors Involved in Visceral Hypersensitivity of Neonatal Maternal Separation Rats

Changes in the intestinal microbiota of healthy adults induced by brown yogurt and relationships of bacterial taxa with specific components.