Z Gastroenterol 2009; 47 - P172
DOI: 10.1055/s-0029-1241422

Immune activation in functional dyspepsia: A result of psychological co-morbidity?

T Liebregts 1, 2, B Adam 1, 2, M Gururatsakul 2, NJ Talley 3, G Gerken 1, G Holtmann 4
  • 1Universitätsklinikum Essen, Gastroenterologie & Hepatologie, Essen, Germany
  • 2Nerve-Gut Research Laboratory, Hanson Institute, Adelaide, Australia
  • 3Mayo Clinic Florida, Division of Gastroenterology, Jacksonville, FL., United States
  • 4Universitätsklinik Essen, Essen, Germany

Aims: Immune activation is believed to play a role in the pathogenesis of IBS (Gastroenterology 2007;132:913–920) but this has not been studied in functional dyspepsia (FD). Psychological factors are associated with altered immunologic function and thus may modulate immune responses in patients with FD.

We hypothesized that the release of cytokines from peripheral blood mononuclear cells (PBMC) is linked to the severity of psychological co-morbidities in patients with FD. Thus we aimed (1) to characterize PBMC mediated cytokine production, (2) the cellular response to lipopolysacharide (LPS) stimulation and (3) to correlate psychological co-morbidities, namely anxiety and depression with immunologic function.

Methods: PBMC from 32 patients with FD and 20 matched controls were isolated by density gradient centrifugation and cultured for 24 hours in RPMI 1640 supplemented with 10% FCS. Basal and E. coli LPS (1ng/ml) stimulated cytokine production (TNF-α, IL-1β, IL-10) of PBMC was measured by enzyme-linked immunosorbent assay (ELISA). Utilizing the standardized Hospital Anxiety and Depression Scale (HADS) 2 subscales of anxiety and depression were calculated. Responders who score ≥11 on either subscale were considered as having a clinically relevant (major) psychological disorder.

Results: Baseline cytokine level (pg/ml) were significantly (p<0.05) increased in FD compared to HC (TNF-α: 115.5±44.9 vs. 58.7±7.4, IL-1β: 225.4±72.5 vs. 80.2±17.4, IL-10: 236.3±62.1 vs. 110.9±18.5) Major anxiety and depression was found in 12 and 9 FD patients, respectively. While baseline cytokine level did not differ between patient groups, LPS- induced IL-1 β and IL-10 level were significantly higher in patients with anxiety (IL-1β: 2425.5±402.8 vs. 1647.8±203.1, IL-10: 1321.1±265.3 vs. 881.7±150) compared to patients without a significant psychological disorder. No significant differences were observed for patients with and without depression.

Conclusions: FD is characterized by increased immune activation. Concomitant anxiety in FD patients is associated with an augmented immunologic response to bacterial antigens. Altered cytokine release may reflect an abnormality in the regulation of immune responses of FD patients, with anxiety being an important co-factor.