Published online Jun 28, 2015. doi: 10.3748/wjg.v21.i24.7362
Peer-review started: January 8, 2015
First decision: January 22, 2015
Revised: February 3, 2015
Accepted: March 12, 2015
Article in press: March 12, 2015
Published online: June 28, 2015
Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder which is characterised by symptoms such as bloating, altered bowel habit and visceral pain. It’s generally accepted that miscommunication between the brain and gut underlies the changes in motility, absorpto-secretory function and pain sensitivity associated with IBS. However, partly due to the lack of disease-defining biomarkers, understanding the aetiology of this complex and multifactorial disease remains elusive. Anecdotally, IBS patients have noted that periods of stress can result in symptom flares and many patients exhibit co-morbid stress-related mood disorders such as anxiety and depression. However, in addition to psychosocial stressors, infection-related stress has also been linked with the initiation, persistence and severity of symptom flares. Indeed, prior gastrointestinal infection is one of the strongest predictors of developing IBS. Despite a lack of overt morphological inflammation, the importance of immune factors in the pathophysiology of IBS is gaining acceptance. Subtle changes in the numbers of mucosal immune cell infiltrates and elevated levels of circulating pro-inflammatory cytokines have been reproducibly demonstrated in IBS populations. Moreover, these immune mediators directly affect neural signalling. An exciting new area of research is the role of luminal microbiota in the modulation of neuro-immune signalling, resulting in local changes in gastrointestinal function and alterations in central neural functioning. Progress in this area has begun to unravel some of the complexities of neuroimmune and neuroendocrine interactions and how these molecular exchanges contribute to GI dysfunction
Core tip: This article assesses the importance of neuroimmune modulation of gastrointestinal function in the functional bowel disorder, irritable bowel syndrome (IBS). Recent progress in understanding the molecular mechanisms underlying the pathophysiology of IBS reveals the neuromodulatory effects of mast cell mediators, cytokines and luminal microbiota.