## 6 Diarrhea to Disorder: Tracing the Path from _Campylobacter jejuni_ Infection to PI-IBS  
PI-IBS manifests as a disturbance in the normal functioning of the gastrointestinal system, marked by abdominal discomfort, bloating and altered defecation patterns, such as diarrhea and constipation [2]. This section traces the trajectory from the initial onset of diarrhea following _C. jejuni_ infection to establishing PI-IBS, exploring the critical transitions that convert an acute gastrointestinal disturbance from the clinical findings. On the other hand, IBD, which includes conditions like [PERSON]'s disease and ulcerative colitis, is distinguished by pronounced inflammation within the digestive tract [2]. This inflammation stems from a complex interplay of genetic predispositions, immune system responses and environmental factors, among which microbial communities play an important but not fully elucidated role. Notably, although IBS and IBD are separate gastrointestinal entities, there exists an intriguing overlap where a subset of individuals with IBD in clinical remission report symptoms characteristic of IBS. Furthermore, in both conditions, episodes following infections have been observed to precipitate disease flare-ups, underscoring a potential common pathway in their pathogenesis linked to post-infectious activation [2]. The association between IBS, microscopic colitis and hyperplasia of enterochromaffin cells is well documented, pinpointing the release of serotonin from these cells as a key factor disrupting normal intestinal movements and altered serotonin pathways, causing increased sensitivity, altered motility, inflammation and enhanced permeability of the gut, characteristic of PI-IBS [1; 29]. The inflammatory condition is reportedly marked by a heightened presence of T-lymphocytes and mast cells, an upsurge in pro-inflammatory cytokine expression and the latter situated near enteric nerve fibers within the gastrointestinal mucosa of affected individuals [67]. The observation indicates that exposure to pathogenic entities disrupting intestinal barrier integrity and altering neuromuscular functionality initiates persistent inflammation, thereby perpetuating the symptoms associated with irritable bowel syndrome. Mucosal inflammation observed in IBS patients frequently correlates with a prior episode of infectious gastroenteritis caused by bacteria, parasites or viruses, leading to what is known as PI-IBS [68]. This connection is reinforced by evidence from various studies, including a meta-analysis highlighting a roughly seven-fold increase in the risk of developing PI-IBS [20; 69]. In the context of acute campylobacteriosis, the primary mechanisms causing diarrhea include sodium malabsorption and a compromised epithelial ion barrier, leading to a condition known as leak-flux diarrhea [70; 71]. The findings explained that diarrhea associated with human campylobacteriosis stems from sodium malabsorption triggered by the invasion of _C. jejuni_. This process is propelled by a cytokine storm mediated by LOS, initiated by the activated cells of the innate immune system [70]. Comprehensive gene expression analyses have identified that pathogenic LOS is the principal regulator of this inflammatory cascade. This regulation leads to the inhibition of sodium channels and precipitates a series of detrimental outcomes, including the compromise of intestinal epithelial barrier integrity, the induction of apoptosis and extensive tissue destruction [70]. Additionally, transporters are involved in the absorption of Na\({}^{+}\) and Cl\({}^{-}\), such as the epithelial sodium channel (ENaC), sodium-hydrogen antiporter 3 (NHE3) and down-regulation in adenoma (DRA), due to their susceptibility to modulation by pro-inflammatory cytokines, a phenomenon also observed in cases of campylobacteriosis [1]. This insight supports the plausible hypothesis that active ion transport mechanisms may undergo up- or down-regulation during and following infectious enteritis caused by _C.