## 5 _C. jejuni's Role in Shaping Microbiota and Contributing to PI-IBS
Specifically, individuals with PI-IBS exhibited a 12-fold increase in the abundance of Bacteroidetes and a substantial decrease of 35 fold in _Firmicutes_ and _Clostridiales_ compared to healthy subjects, highlighting the significant microbial shifts associated with PI-IBS development [10; 59]. The effects of the intestinal microbiota on human health and disease is well recognized, and though research in the last decade has not pinpointed a direct cause-and-effect relationship with a singular pathogen, numerous studies have indicated that individuals with IBD or IBS tend to have a lower presence of protective, anti-inflammatory bacteria alongside a higher prevalence of aggressive, pro-inflammatory bacteria [2]. Notably, levels of _Faecalibacterium prausnitzii_, belonging to the _Firmicutes_ phylum, considered a probiotic bacterium and known for its anti-inflammatory properties, have been found to be diminished in cases of IBD [2; 60]. On the other hand, Proteobacteria, especially the abundance of _E. coli_, are notably higher in patients with [PERSON]'s disease, illustrating the significant but complex role of gut microbiota composition in developing and exacerbating these conditions [2]. In PI-IBS, there is a noted increase in the _Firmicutes_-_Bacteroides_ ratio alongside a reduction in microbial diversity [30]. Such shifts can significantly alter the luminal environment through changes in the composition of bile acids, bile salts and proteases, leading to bile acid malabsorption in PI-IBS patients, a known trigger for diarrhea [10]. Proteases play a crucial role in mediating intestinal barrier dysfunction and visceral hypersensitivity, which are strongly linked to IBS. Elevated levels of fecal proteolytic activity were correlated with increased symptom severity and reduced microbial diversity in patients with _C. jejuni_-induced PI-IBS [10]. Commensal microbes can synthesize \(\beta\)-glucuronidases, inhibiting the host's proteolytic activity and consequently protecting the intestinal epithelium [61]. This observation has led to the hypothesis that a reduction in microbial \(\beta\)-glucuronidase enzymatic activity could play a role in developing IBS. Additionally, enhanced density of enteroendocrine cells and a subsequent increased release of serotonin may impact intestinal motility. For up to a year following the initial _Campylobacter_ infection, individuals who develop PI-IBS can exhibit an acute rise in the number of enteroendocrine cells and T lymphocytes, along with increased gut permeability [58]. The cytotoxic impact of _CdB_, produced by C. _jejuni_, can reduce the number of ICCs and induce alterations in the gut microbiome, explaining the pathophysiology of PI-IBS in the initial stages following infection [28]. However, the enduring nature of PI-IBS symptoms, persisting for as long as eight years post-infection for some patients, remains challenging to elucidate solely based on these mechanisms. Additionally, the phenomenon where some individuals experience a symptom-free interval between the initial _Campylobacter_ infection and the subsequent development of IBS symptoms adds another layer of complexity. This suggests that additional factors, including immune system modulation, genetic predisposition or further changes in the gut microbiota over time, might contribute to prolonged and delayed symptomatology in some cases of post-_Campylobacter_ post-sequelae [28]. In an intriguing study with experimental PI-IBS rats, the administration of _Lactobacillus rhamous_ GG supernatant increased the expression of serotonin reuptake transporter (SERT) messenger RNA and protein within the colon [62]. Through probiotic intervention, microbial modulation can rectify the serotonergic imbalance observed in PI-IBS. Recent clinical research has uncovered that patients with constipation-predominant IBS-C exhibit a correlation between fecal concentrations of _Lactobacillus_ and _Bifidobacterium_ and levels of interleukin IL-10, an anti-inflammatory cytokine [63].