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Clinical Trial
. 2016 May 26;11(5):e0156387.
doi: 10.1371/journal.pone.0156387. eCollection 2016.

Serum Fatty Acids Are Correlated with Inflammatory Cytokines in Ulcerative Colitis

Dawn M Wiese  1   2 , Sara N Horst  1   2 , Caroline T Brown  2 , Margaret M Allaman  2 , Mallary E Hodges  3 , James C Slaughter  4 , Jennifer P Druce  2   5 , Dawn B Beaulieu  2 , David A Schwartz  2 , Keith T Wilson  1   2   6   7 , Lori A Coburn  1   2
Affiliations
Clinical Trial

Serum Fatty Acids Are Correlated with Inflammatory Cytokines in Ulcerative Colitis

Dawn M Wiese et al. PLoS One. .

Abstract

Background and aims: Ulcerative colitis (UC) is associated with increased dietary intake of fat and n-6 polyunsaturated fatty acids (PUFA). Modification of fat metabolism may alter inflammation and disease severity. Our aim was to assess differences in dietary and serum fatty acid levels between control and UC subjects and associations with disease activity and inflammatory cytokines.

Methods: Dietary histories, serum, and colonic tissue samples were prospectively collected from 137 UC subjects and 38 controls. Both histologic injury and the Mayo Disease Activity Index were assessed. Serum and tissue cytokines were measured by Luminex assay. Serum fatty acids were obtained by gas chromatography.

Results: UC subjects had increased total fat and oleic acid (OA) intake, but decreased arachidonic acid (AA) intake vs controls. In serum, there was less percent saturated fatty acid (SFA) and AA, with higher monounsaturated fatty acids (MUFA), linoleic acid, OA, eicosapentaenoic acid (EPA), and docosapentaenoic acid (DPA) in UC. Tissue cytokine levels were directly correlated with SFA and inversely correlated with PUFA, EPA, and DPA in UC subjects, but not controls. 5-aminosalicylic acid therapy blunted these associations.

Conclusions: In summary, we found differences in serum fatty acids in UC subjects that correlated with pro-inflammatory tissue cytokines. We propose that fatty acids may affect cytokine production and thus be immunomodulatory in UC.

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Conflict of interest statement

Competing Interests: DAS has consultancy agreements with Abbvie, UCB, Janssen, Takeda, and Tigenix and is currently receiving grants from Abbvie and UCB. However, these agreements and grants had no relationship to the current research study. KTW has had a consulting agreement with Immune Pharmaceuticals. However, this agreement had no relationship to the current research study and is no longer active. The remainder of the authors declare that they have no conflict of interest. This does not alter the authors’ adherence to PLOS ONE policies on sharing data and materials.

Figures

Fig 1
Fig 1. Detailed analysis of serum fatty acids by histologic disease activity.
Blood was obtained from each subject and processed within 30 min to obtain serum. Serum fatty acid levels were measured as described in the Methods. Disease categories were based on maximal tissue histopathology. n = 23 for control (Ctrl) and n = 101 for UC subjects. *P < 0.05, **P < 0.01, ***P < 0.001 versus control.
Fig 2
Fig 2. Tissue cytokines are directly correlated with serum percent SFA.
Snap frozen colonic biopsies were lysed and cytokine/chemokine levels were measured by Luminex technology, with each sample corrected for tissue lysate protein concentration, as described in the Methods. Blood was obtained from each subject and processed within 30 min to obtain serum. Serum fatty acid levels were measured as described in the Methods. The Spearman correlation coefficient (r) and the associated P value are shown. n = 58 for UC subjects. There were no significant correlations in control subjects (data not shown).
Fig 3
Fig 3. Tissue cytokines are inversely correlated with percent serum PUFA, EPA, and DPA.
Snap frozen colonic biopsies were lysed and cytokine/chemokine levels were measured by Luminex technology, with each sample corrected for tissue lysate protein concentration, as described in the Methods. Blood was obtained from each subject and processed within 30 min to obtain serum. Serum fatty acid levels were measured as described in the Methods. The Spearman correlation coefficient (r) and the associated P value are shown. (A–C) Inverse correlations with percent serum PUFA. (D–F) Inverse correlations with percent serum EPA. (G) Inverse correlation with percent serum DPA. n = 58 for UC subjects. There were no significant correlations in control subjects (data not shown).
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