Colitis is commonly described as a chronic inflammatory condition of the colon, characterised by recurring episodes of abdominal pain, diarrhoea, rectal bleeding, fatigue, and impaired quality of life. It is typically framed as an autoimmune or immune-mediated disorder, in which the body’s immune system is believed to attack the lining of the large intestine. Clinical management has therefore focused primarily on suppressing inflammation and controlling immune activity, often with the expectation that the condition is lifelong and progressive.

This framing has shaped medical practice, patient education, and research priorities for decades. Colitis is often presented as a disease of flares and remissions, managed rather than resolved, with treatment strategies aimed at maintaining symptom control rather than restoring underlying biological balance. While this approach has provided relief for many individuals, it has also left significant questions unanswered regarding disease variability, long-term outcomes, and the fundamental mechanisms driving chronic inflammation in the gut.

Despite extensive research, colitis remains a heterogeneous condition. Patients with similar diagnoses may experience markedly different symptom patterns, disease severity, progression rates, and responses to treatment. Some individuals experience mild, intermittent symptoms, while others face severe, persistent inflammation with systemic consequences. This variability suggests that colitis may not represent a single disease entity, but rather a spectrum of biological states converging on a shared clinical presentation.

Traditional models of colitis centre on dysregulated immune responses within the intestinal mucosa. Histological findings often reveal infiltration of immune cells, disruption of epithelial architecture, ulceration, and increased production of pro-inflammatory cytokines. These features are interpreted as evidence of immune overactivity directed against intestinal tissue. However, this perspective raises an important question: why does the immune system behave this way in the first place?

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