{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,1]],"date-time":"2026-11-01T03:49:55Z","timestamp":1793504995576,"version":"4.5.0"},"reference-count":316,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2021,5,5]],"date-time":"2021-05-05T00:00:00Z","timestamp":1620172800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["ssph-journal.org"],"crossmark-restriction":true},"short-container-title":["Public Health Rev"],"abstract":"<jats:p>\n                    <jats:bold>Objective:<\/jats:bold>\n                    Inflammatory bowel diseases (IBDs) are complex chronic inflammatory disorders of the gastro-intestinal (GI) tract with uncertain etiology. IBDs comprise two idiopathic disorders: Crohn\u2019s disease (CD) and ulcerative colitis (UC). The aetiology, severity and progression of such disorders are still poorly understood but thought to be influenced by multiple factors (including genetic, environmental, immunological, physiological, psychological factors and gut microbiome) and their interactions. The overarching aim of this review is to evaluate the extent and nature of the interrelationship between these factors with the disease course. A broader conceptual and longitudinal framework of possible neuro-visceral integration, core microbiome analysis and immune modulation assessment may be useful in accurately documenting and characterizing the nature and temporal continuity of crosstalk between these factors and the role of their interaction (s) in IBD disease activity. Characterization of these interactions holds the promise of identifying novel diagnostic, interventions, and therapeutic strategies.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Material and Methods:<\/jats:bold>\n                    A search of published literature was conducted by exploring PubMed, EMBASE, MEDLINE, Medline Plus, CDSR library databases. Following search terms relating to key question were set for the search included: \u201cInflammatory bowel diseases,\u201d \u201cgut microbiota,\u201d \u201cpsychological distress and IBD,\u201d \u201cautonomic reactivity and IBD,\u201d \u201cimmune modulation,\u201d \u201cchronic inflammation,\u201d \u201cgut inflammation,\u201d \u201centeric nervous system,\u201d \u201cgut nervous system,\u201d \u201cCrohn\u2019s disease,\u201d \u201cUlcerative colitis\u201d, \u201cdepression and IBD\u201d, \u201canxiety and IBD\u201d, \u201cquality of life in IBD patients,\u201d \u201crelapse in IBDs,\u201d \u201cremission in IBDs,\u201d \u201cIBD disease activity,\u201d \u201cbrain-gut-axis,\u201d \u201cmicrobial signature in IBD,\u201d \u201cvalidated questionnaires in IBD,\u201d \u201cIBD activity indices,\u201d \u201cIBD aetiology,\u201d \u201cIBDs and stress,\u201d \u201cepidemiology of IBDs\u201d, \u201cautonomic nervous system and gut inflammation\u201d, \u201cIBD and environment,\u201d \u201cgenetics of IBDs,\u201d \u201cpathways of immune response in IBDs,\u201d \u201csleep disturbances in IBD,\u201d \u201chypothalamic-pituitary-adrenal axis (HPA),\u201d \u201csympatho-adrenal axis,\u201d \u201cCNS and its control of gut function\u201d \u201cmucosal immune response,\u201d \u201ccommensal and pathogenic bacteria in the gut,\u201d \u201cinnate and adaptive immunity.\u201d Studies evaluating any possible associations between gut microbiome, psychological state, immune modulation, and autonomic function with IBDs were identified. Commonly cited published literatures with high quality research methodology\/results and additional articles from bibliographies of recovered papers were examined and included where relevant.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results:<\/jats:bold>\n                    Although there is a substantial literature identifying major contributing factors with IBD, there has been little attempt to integrate some factors over time and assess their interplay and relationship with IBD disease activity. Such contributing factors include genetic and environmental factors, gut microbiota composition and function, physiological factors, psychological state and gut immune response. Interdependences are evident across psychological and biological factors and IBD disease activity. Although from the available evidence, it is implausible that a single explanatory model could elucidate the interplay between such factors and the disease course as well as the sequence of the effect during the pathophysiology of IBD.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion:<\/jats:bold>\n                    Longitudinal monitoring of IBD patients and integrating data related to the contributing\/risk factors including psychological state, physiological conditions, inflammatory\/immune modulations, and microbiome composition\/function, could help to explain how major factors associate and interrelate leading to exacerbation of symptoms and disease activity. Identifying the temporal trajectory of biological and psychosocial disturbances may also help to assess their effects and interdependence on individuals\u2019 disease status. Moreover, this allows greater insight into understanding the temporal progressions of subclinical events as potential ground for disease severity in IBD. Furthermore, understanding the interaction between these risk factors may help better interventions in controlling the disease, reducing the costs related to disease management, further implications for clinical practice and research approaches in addition to improving patients\u2019 mental health and quality of life.\n                  <\/jats:p>","DOI":"10.3389\/phrs.2021.1603990","type":"journal-article","created":{"date-parts":[[2021,8,11]],"date-time":"2021-08-11T13:05:01Z","timestamp":1628687101000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":159,"title":["A Review of Inflammatory Bowel Disease: A Model of Microbial, Immune and Neuropsychological Integration"],"prefix":"10.3389","volume":"42","author":[{"given":"P.","family":"Tavakoli","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"U.","family":"Vollmer-Conna","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.","family":"Hadzi-Pavlovic","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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