## 3 Results
### Signalling Pathway  
Cells can interact and coordinate their activities through the intricate networks of chemicals and events known as signalling pathways. Cellular characteristics, such as growth, proliferation, and apoptosis, are ultimately influenced by the information they receive from internal or external stimuli. Errors in these pathways can result in diseases since they are essential for immunity, homeostasis, tissue repair, and development. Complex networks of molecular interactions known as signalling pathways transmit signals from cell surface receptors to intracellular effectors, which in turn influence cellular processes, such as differentiation, death, and proliferation. These signalling pathways are appealing candidates for therapeutic intervention because they are frequently dysregulated in a variety of illnesses, such as cancer [135], autoimmune diseases, and metabolic disorders [136]. Disruptions in the gut-brain axis, where the stomach and brain communicate via a variety of signalling pathways, are a component of IBS. These include the vagus nerve, the Toll-like receptor 4 (TLR4) pathway, the 5-HT signalling pathway, the MAPK pathway, mechanistic target of rapamycin (mTOR) signalling, and nuclear factor-kappa-B (NF-\(\kappa\)B) signalling pathways (Figure 5). Symptoms like bloating, changed bowel habits, and stomach pain might result from the dysregulation of these circuits. Multiple bidirectional routes involving immunological, endocrine, and neurological transmission connect the gut microbiota to the central nervous system. Neurotransmitters and digestive hormones that change the brain and behaviour can be produced by gastrointestinal tract cells under the influence of the microbiota [137; 138]. In order to influence behaviour, they can also stimulate the vagus nerve, alter local immune populations that travel to the central nervous system, and release neuroactive compounds into the bloodstream [139; 140]. Through adrenergic nerve transmission, which mainly affects intestinal motility, and the neurotransmitter effect on immunological mediators that influence microbiota composition and function, the central nervous system can regulate the gut microbiota [87]. Neuronal growth, brain function, cognitive regulation, and aging are all impacted by the \"gut-brain axis,\" a two-way communication system between the gut microbiota and the brain [141]. The central nervous, endocrine, and immunological systems are all part of the gut-brain axis, which is a network of information transmission between the gut and the brain [15; 140]. The Toll-like receptor 4 is crucial for the development of IBS, according to a growing body of research in recent years [142; 143]. As members of the transmembrane pattern recognition receptor family, Toll-like receptor 4 crosses the gap between innate and acquired immunity and is crucial for innate immune responses. Mucosal immune response, barrier function, cell adhesion, proliferation, migration, pathogen defence, epithelial cell injury healing, and other processes are all impacted by Toll-like receptor 4 [144]. Therefore, the formation and progression of various disorders, including autoimmune diseases, cancer, infections, and chronic inflammation, are facilitated by the deregulation of the Toll-like receptor 4 signalling pathway [145]. The development of IBD is significantly influenced by the production of proinflammatory cytokines, including as interleukin (IL)-1, IL-6, IL-17, IL-22, IL-23, TNF-\(\alpha\), and interferon-\(\gamma\) (IFN-\(\gamma\)) [146]. Certain amino acids (Table 1) may be potential biomarkers for the early diagnosis and treatment of ulcerative colitis patients, as evidenced by the different metabolic profiles of  
Figure 5: Signalling pathways affecting IBS. We created this image with Canva. amino acids in ulcerative colitis [147]. Additionally, recent research indicates that amino acids play important roles in intestinal inflammation.