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Cytokine profiling of pancreatic fluid using the ePFT collection method in tandem with a multiplexed microarray assay
Joao A Paulo1, Linda S Lee, Bechien Wu
1Department of Pathology, Children's Hospital Boston, Boston, MA, United States.
Insights
Researchers identified specific cytokine differences in pancreatic fluid from patients with chronic pancreatitis (CP) compared to chronic abdominal pain (CAP) controls. This finding aids understanding of pancreatic immune responses and fibrosis in CP.
Area of Science:
- Immunology
- Gastroenterology
- Biochemistry
Background:
- Cytokines are key immunomodulators influencing pancreatic stellate cell activation and fibrosis in chronic pancreatitis (CP).
- Identifying specific cytokine profiles in pancreatic fluid could elucidate CP pathogenesis.
Purpose of the Study:
- To determine if cytokines can be identified in pancreatic fluid using the endoscopic pancreatic fluid collection (ePFT) method.
- To compare cytokine profiles between CP patients and chronic abdominal pain (CAP) controls.
Main Methods:
- Pancreatic fluid was collected endoscopically from CP and CAP patients using the ePFT method.
- Fluid samples underwent multiplexed cytokine protein microarray analysis.
- Secretin-stimulated ePFT was performed, measuring peak bicarbonate concentrations.
Main Results:
- Significant decreases in specific cytokines (EGF, IP-10, eotaxin, IL-3, MIP-1a, IL-15, PDGF-AB/BB, IL-1a) were observed in CP patients compared to CAP controls (p<0.05).
- Distinct cytokine abundance differences were successfully identified in ePFT-collected pancreatic fluid.
Conclusions:
- The ePFT method combined with microarray analysis effectively identifies cytokine differences in pancreatic fluid.
- These findings advance the understanding of immune responses and pathogenesis in chronic pancreatitis.
Abstract:
Cytokines are secreted immunomodulating proteins involved in pancreatic stellate cell activation and propagation of fibrosis in chronic pancreatitis. We aim to show that cytokines can be identified from pancreatic fluid by (1) collecting pancreatic fluid with the ePFT method, (2) processing the fluid for cytokine-targeted microarray analysis, and (3) comparing cytokine profiles in pancreatic fluid of chronic pancreatitis (CP) patients and of chronic abdominal pain (CAP) controls. We endoscopically collected pancreatic fluid from patients with CP and those with CAP using the ePFT method. This fluid was subjected directly to a multiplexed cytokine protein microarray assay. Six patients (3 CP, 3 CAP) underwent a secretin-stimulated ePFT. The mean peak bicarbonate concentrations [meq/L] of the CP and CAP patients were 43 and 97, respectively. Statistically significant decreases in the cytokine concentrations of EGF, IP-10, eotaxin, IL-3, MIP-1a, IL-15, PDGF-AB/BB, and IL-1a were observed in the CP specimens (p<0.05). We have successfully identified differences in the abundance of cytokines in ePFT-collected pancreatic fluid with a multiplexed microarray assay comparing CP and CAP controls. Further targeted investigation of cytokines in ePFT-collected fluid will broaden our knowledge of pancreatic immune response and pathogenesis in chronic pancreatitis.
