## 3 Results
### The Role of the Enteric Nervous System in IBS
Following this, a study [104] that analysed 5-HT levels in platelet-depleted plasma revealed that patients with IBS who experienced constipation had a lower 5-HT release following a typical meal when compared to those with post-infectious IBS and healthy people. Additionally, post-infectious IBS patients had a higher peak in postprandial 5-HT than either patient with constipation IBS symptoms or healthy controls. Another team of researchers found comparable results in healthy individuals who were fed and stopped eating, as well as IBS patients who had either diarrhoea or constipation symptoms. Furthermore, patients with constipation symptoms had a 5-HIAA/5-HT ratio within a normal range, while those with IBS who also experienced diarrhoea had a lower 5-HIAA/5-HT ratio [105]. This suggests that patients with diarrhoea may have a decreased 5-HT reuptake, while those with IBS who experience constipation are likely to have a reduced 5-HT release. Several studies have looked at the relationship between intestinal barrier function, mucosal inflammation, immunological activation, and 5-HT metabolism. According to Cremon [106], 5-HT-positive enterochromaffin cells are more frequent in colonic biopsies from IBS patients than in biopsies from healthy controls; actually, this proportion was higher in IBS patients who experienced diarrhoea symptoms than in those who suffered from constipation symptoms. In this study, mucosal 5-HT was likewise significantly higher in IBS patients, and it was correlated with both a degree of stomach pain and mast-cell numbers. Serotonin is predominantly secreted in the gastrointestinal tract. Intestinal periodic pulsatile distension promotes its release from mucosal cells [107,108]. 5-HT activates the 5-HT3 and 5-HT4 receptors found in the intrinsic primary afferent neurons of the enteric nervous system, mediating secretory and motor responses in the gastrointestinal tract and innervating smooth muscles [109]. 5-HT influences the lipo-polysaccharide-triggered release of several pro-inflammatory cytokines, including interleukin-1\(\beta\) (IL-1\(\beta\)), IL-6, IL-8/CXCL8, IL-12, and tumour necrosis factor \(\alpha\) (TNF\(\alpha\)) [110]. Among them, IL-1\(\beta\) is a cytokine that promotes inflammation. It is expressed at high levels in response to various stimuli. Produced mainly by leukocytes, IL-1\(\beta\) modulates the function of both immune (dendritic cells, macrophages, and neutrophils) and non-immune cells (Figure 4) [111]. The pathophysiology of inflammatory bowel disease (IBD) consists of two primary components: the deterioration of intestinal epithelial integrity due to heightened pro-inflammatory mediators, and a dysfunction in the intestinal immune system that resultsin chronic inflammation from immune cell aggregation and microbiota imbalance [112]. Traditional treatments for IBD, guided by pathological and physiological symptoms, focus on diminishing inflammation and attenuating the immune response through medications like 5-aminosalicylic acid (5-ASA), corticosteroids, immunosuppressive, antibiotics, or anti-TNF biological agents [113; 114; 115]. The first-line treatment for IBD consists of aminoasiclylates, then corticosteroids, and subsequently immunosuppressive. Additionally, antibiotics (such as ciprofloxacin and rifampicin) and probiotics (like _bifidobacterium_ spp. and _lactobacillus_ spp.) are employed to correct imbalances in the gut microbiota. Should these treatments not adequately manage inflammation, surgical options like colorectal resection might be required [116]. Concerning the treatment methods mentioned above, clinical studies have shown that the long-term use of medications like 5-ASA can lead to serious side effects, including cytotoxic effects on healthy cells [117]. During IBD, epithelial cells and activated macrophages exhibit the overexpression of specific antigens or receptors, including mannose receptors, interleukin like IL-1\(\beta\), and chemokines [118].