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Functional Bowel Disorders Are Associated with a Central Immune Activation

BACKGROUND: Subjects with depression and unexplained neurological symptoms have a high prevalence of gastrointestinal comorbidity probably related to the brain-gut communication. This study explored associations between functional gastrointestinal disorders (FGID) and inflammatory markers in subject...

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Detalles Bibliográficos
Autores principales: Farup, Per G., Ueland, Thor, Rudi, Knut, Lydersen, Stian, Hestad, Knut
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5672610/
https://www.ncbi.nlm.nih.gov/pubmed/29201045
http://dx.doi.org/10.1155/2017/1642912
Descripción
Sumario:BACKGROUND: Subjects with depression and unexplained neurological symptoms have a high prevalence of gastrointestinal comorbidity probably related to the brain-gut communication. This study explored associations between functional gastrointestinal disorders (FGID) and inflammatory markers in subjects with these disorders. METHODS: The FGID, including irritable bowel syndrome (IBS), were classified according to the Rome III criteria, and degree of symptoms was assessed with IBS symptom severity score (IBS-SSS). A range of interleukins (IL), chemokines and growth factors, tryptophan, and kynurenine were analysed in serum and the cerebrospinal fluid (CSF), and short-chain fatty acids (SCFA) were analysed in the faeces. The results are reported as partial correlation (pc) and p values. RESULTS: Sixty-six subjects were included. IBS was associated with high levels of tryptophan (p = 0.048) and kynurenine (p = 0.019) and low level of IL-10 (p = 0.047) in the CSF. IBS-SSS was associated with high tumor necrosis factor and low IL-10 in the CSF; pc = 0.341 and p = 0.009 and pc = −0.299 and p = 0.023, respectively. Propionic minus butyric acid in faeces was negatively associated with IL-10 in the CSF (pc = −0.416, p = 0.005). CONCLUSIONS: FGID were associated with a proinflammatory immune activation in the central nervous system and a disturbed tryptophan metabolism that could have been mediated by the faecal microbiota.