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The Initiating Immune Response of Acute Pancreatitis May be Mediated by the T-Helper 17 Pathway

Patti S Kay, Martin Smith, Martin Brand

Objectives Acute pancreatitis is characterized by a systemic inflammatory response. We hypothesized that the fundamental inflammatory response observed during the initial stages of all acute pancreatitis is not a Th1 but rather a Th17 response. Methods Seven patients with mild AP presenting within three days of symptom onset were recruited. Peripheral blood was drawn for five consecutive days and plasma Th1/Th2/Th17 cytokine levels compared to eleven healthy controls. Plasma cytokine measurements were performed using Th1/ Th2/Th17 Cytokine Bead Array assay and data quantified using FCAP Array software. Results IL-6 levels were significantly elevated in AP patients compared to controls; IL-10 levels were significantly elevated by day 3; IL17A levels increased on day 2 and significantly elevated at day 3 compared to controls declining to non-significant levels by day 4. IFNγ and TNFα levels were low at all time-points. Conclusion IL-17A and IL-10 (an anti-inflammatory cytokine implicated in suppressing Th17 cytokines secreted by macrophages and T cells) were elevated by day 3. In addition IL-6, which helps drive development of Th17 cells, was significantly elevated at all time-points. These preliminary results imply that the underlying AP induced systemic inflammation is polarized to a Th17 rather than a Th1 response.