Type your tag names separated by a space and hit enter

Immune activation in patients with irritable bowel syndrome.

Abstract

BACKGROUND AND AIMS

We set out to test the hypothesis that irritable bowel syndrome (IBS) is characterized by an augmented cellular immune response with enhanced production of proinflammatory cytokines. We further aimed to explore whether symptoms and psychiatric comorbidity in IBS are linked to the release of proinflammatory cytokines.

METHODS

We characterized basal and Escherichia coli lipopolysaccharide (LPS)-induced cytokine production in peripheral blood mononuclear cells (PBMCs) from 55 IBS patients (18 mixed-, 17 constipation-, 20 diarrhea-predominant) and 36 healthy controls (HCs). PBMCs were isolated by density gradient centrifugation and cultured for 24 hours with or without (1 ng/mL) LPS. Cytokine production (tumor necrosis factor [TNF]-alpha, interleukin [IL]-1beta, and IL-6) was measured by enzyme-linked immunosorbent assay. Abdominal symptoms and psychiatric comorbidities were assessed by using the validated Bowel Disease Questionnaire and the Hospital Anxiety and Depression Scale.

RESULTS

IBS patients showed significantly (P < .017) higher baseline TNF-alpha, IL-1beta, IL-6, and LPS-induced IL-6 levels compared with HCs. Analyzing IBS subgroups, all cytokine levels were significantly (P < .05) higher in diarrhea-predominant IBS (D-IBS) patients, whereas constipation-predominant IBS patients showed increased LPS-induced IL-1beta levels compared with HCs. Baseline TNF-alpha and LPS-induced TNF-alpha and IL-6 levels were significantly higher in patients reporting more than 3 bowel movements per day, urgency, watery stools, and pain associated with diarrhea compared with patients without these symptoms (all P < .05). LPS-induced TNF-alpha production was associated significantly (r = 0.59, P < .001) with anxiety in patients with IBS.

CONCLUSIONS

Patients with D-IBS display enhanced proinflammatory cytokine release, and this may be associated with symptoms and anxiety.

Links

  • Publisher Full Text
  • Authors+Show Affiliations

    ,

    Department of Gastroenterology and Hepatology, University of Adelaide, Royal Adelaide Hospital, South Australia, Australia.

    , , , , , , , , ,

    Source

    Gastroenterology 132:3 2007 Mar pg 913-20

    MeSH

    Adult
    Anxiety
    Case-Control Studies
    Cells, Cultured
    Cytokines
    Depression
    Enzyme-Linked Immunosorbent Assay
    Female
    Humans
    Immunity, Cellular
    Inflammation Mediators
    Interleukin-1beta
    Interleukin-6
    Irritable Bowel Syndrome
    Leukocytes, Mononuclear
    Lipopolysaccharides
    Male
    Psychiatric Status Rating Scales
    Severity of Illness Index
    Surveys and Questionnaires
    Tumor Necrosis Factor-alpha

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    17383420

    Citation

    Liebregts, Tobias, et al. "Immune Activation in Patients With Irritable Bowel Syndrome." Gastroenterology, vol. 132, no. 3, 2007, pp. 913-20.
    Liebregts T, Adam B, Bredack C, et al. Immune activation in patients with irritable bowel syndrome. Gastroenterology. 2007;132(3):913-20.
    Liebregts, T., Adam, B., Bredack, C., Röth, A., Heinzel, S., Lester, S., ... Holtmann, G. (2007). Immune activation in patients with irritable bowel syndrome. Gastroenterology, 132(3), pp. 913-20.
    Liebregts T, et al. Immune Activation in Patients With Irritable Bowel Syndrome. Gastroenterology. 2007;132(3):913-20. PubMed PMID: 17383420.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Immune activation in patients with irritable bowel syndrome. AU - Liebregts,Tobias, AU - Adam,Birgit, AU - Bredack,Christoph, AU - Röth,Alexander, AU - Heinzel,Susanne, AU - Lester,Sue, AU - Downie-Doyle,Sarah, AU - Smith,Eric, AU - Drew,Paul, AU - Talley,Nicholas J, AU - Holtmann,Gerald, Y1 - 2007/01/26/ PY - 2006/04/05/received PY - 2006/12/07/accepted PY - 2007/3/27/pubmed PY - 2007/4/27/medline PY - 2007/3/27/entrez SP - 913 EP - 20 JF - Gastroenterology JO - Gastroenterology VL - 132 IS - 3 N2 - BACKGROUND AND AIMS: We set out to test the hypothesis that irritable bowel syndrome (IBS) is characterized by an augmented cellular immune response with enhanced production of proinflammatory cytokines. We further aimed to explore whether symptoms and psychiatric comorbidity in IBS are linked to the release of proinflammatory cytokines. METHODS: We characterized basal and Escherichia coli lipopolysaccharide (LPS)-induced cytokine production in peripheral blood mononuclear cells (PBMCs) from 55 IBS patients (18 mixed-, 17 constipation-, 20 diarrhea-predominant) and 36 healthy controls (HCs). PBMCs were isolated by density gradient centrifugation and cultured for 24 hours with or without (1 ng/mL) LPS. Cytokine production (tumor necrosis factor [TNF]-alpha, interleukin [IL]-1beta, and IL-6) was measured by enzyme-linked immunosorbent assay. Abdominal symptoms and psychiatric comorbidities were assessed by using the validated Bowel Disease Questionnaire and the Hospital Anxiety and Depression Scale. RESULTS: IBS patients showed significantly (P < .017) higher baseline TNF-alpha, IL-1beta, IL-6, and LPS-induced IL-6 levels compared with HCs. Analyzing IBS subgroups, all cytokine levels were significantly (P < .05) higher in diarrhea-predominant IBS (D-IBS) patients, whereas constipation-predominant IBS patients showed increased LPS-induced IL-1beta levels compared with HCs. Baseline TNF-alpha and LPS-induced TNF-alpha and IL-6 levels were significantly higher in patients reporting more than 3 bowel movements per day, urgency, watery stools, and pain associated with diarrhea compared with patients without these symptoms (all P < .05). LPS-induced TNF-alpha production was associated significantly (r = 0.59, P < .001) with anxiety in patients with IBS. CONCLUSIONS: Patients with D-IBS display enhanced proinflammatory cytokine release, and this may be associated with symptoms and anxiety. SN - 0016-5085 UR - https://www.unboundmedicine.com/medline/citation/17383420/full_citation L2 - https://linkinghub.elsevier.com/retrieve/pii/S0016-5085(07)00185-0 DB - PRIME DP - Unbound Medicine ER -