Biomarkers of Emotional Distress in Irritable Bowel Syndrome (IBS)

Evidence highlights the comorbidity between emotional distress and Irritable bowel syndrome (IBS) through the brain-gut microbiome axis. However, the underlying mechanism is largely unknown, and limited studies have addressed the role of the gut microbiome and the neurotransmitters in this comorbidity. The study aimed to identify biomarkers of emotional distress (neurotransmitter levels and gut microbiome patterns) in individuals with IBS. In this cross-sectional study, 28 individuals with IBS and ten healthy controls were assessed for their level of emotional distress, including anxiety and depression. Plasma neurotransmitters(serotonin, norepinephrine) were tested using the enzyme-linked immunosorbent assay (ELISA) method. Fecal samples were collected, and gut microbiome profiles were examined using 16S rRNA Illumina sequencing. The microbial analyses comprised of alpha and beta diversity as well as bacterial composition. The Pearson correlation used to investigate the relationship between neurotransmitters levels and bacterial profile. The emotional distress was significantly different between IBS and healthy control groups. However, the levels of the neurotransmitters, including serotonin and norepinephrine, were not different between the two groups. While the bacterial profiles differed between IBS and healthy controls, there was no significant association between neurotransmitter levels and bacterial profile except negative correlation between plasma serotonin levels and total observed species (sobs) as well as positive correlation association between plasma serotonin levels and beta diversity. The present study demonstrated that the bacterial composition of fecal samples of participants with IBS was different from healthy controls. While there was no difference in neurotransmitter levels between study groups, the correlation between gut microbiome diversity and plasma serotonin levels suggests that the pattern of the gut microbiome may impact the neurotransmitter levels. Further studies are required to specify the involved gut microbiota in the modulation of the neurotransmitter levels

Associations of inflammation with neuropsychological symptom cluster in patients with Head and neck cancer: A longitudinal study

Purpose: Head and neck cancer (HNC) patients may experience multiple co-occurring neuropsychological symptoms (NPS) cluster, including fatigue, depression, pain, sleep disturbance, and cognitive impairment. While inflammation has been attributed as a key mechanism for some of these symptoms, its association with the NPS as a cluster of symptoms is unknown. Thus, the aim of this study was to examine the association between peripheral inflammation and NPS cluster among HNC patients over cancer treatment (radiotherapy with or without chemotherapy). Methods: HNC patients were recruited and followed at pre-treatment, end of treatment, three months and one-year post-treatment. Plasma inflammatory markers, including C-reactive protein (CRP), tumor necrosis factor-alpha (TNFA), soluble tumor necrosis factor receptor-2 (sTNFR2), interleukin-1 beta (IL1-β), interleukin-6 (IL-6), interleukin-10 (IL-10), monocyte chemotactic protein-1 (MCP-1), and interleukin-1 receptor antagonist (IL-1RA) and patient-reported NPS cluster were collected at the 4 time points. Associations between inflammatory markers and the NPS cluster were analyzed using linear mixed-effects models and generalized estimating equations (GEE) models controlling covariates. Results: 147 HNC patients were eligible for analysis. 56% of the patients received chemoradiotherapy as treatment. The highest NPS cluster score was reported at the end of treatment, which gradually decreased over time. An increase in inflammatory markers including CRP, sTNFR2, IL-6 and IL-1RA was associated with higher continuous NPS cluster scores (p<0.001, p = 0.003, p<0.001, p<0.001; respectively). GEE further confirmed that patients with at least two moderate symptoms had elevated sTNFR2, IL-6, and IL-1RA (p = 0.017, p = 0.038, p = 0.008; respectively). Notably, this positive association between NPS cluster and inflammatory markers was still significant at one-year post-treatment for CRP (p = 0.001), sTNFR2 (p = 0.006), and IL-1RA (p = 0.043). Conclusions: Most HNC patients experienced NPS clusters over time, especially immediately after the end of treatment. Elevated inflammation, as represented by inflammatory markers, was strongly associated with worse NPS cluster over time; this trend was also notable at one-year post-treatment. Our findings suggest that peripheral inflammation plays a pivotal role in the NPS cluster over cancer treatment, including long-term follow-ups. Interventions on reducing peripheral inflammation may contribute to alleviating the NPS cluster in cancer patients