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Author Notes:

To whom correspondence may be addressed. Email: wxh64@psu.edu or afriedman@ math.osu.edu

W.H., D.L.C., and G.B.L. designed research

W.H., G.B.L., and A.F. performed research

H.M.K. contributed new reagents/analytic tools

W.H., H.M.K., P.A.H., and G.B.L. analyzed data

W.H., G.B.L., and A.F. wrote the paper.

Reviewers: F.S.G., Yale University School of Medicine; and Y.K., Arizona State University.

The authors declare no conflict of interest.

Subjects:

Research Funding:

W.H. and A.F. have been supported by the Mathematical Biosciences Institute and the National Science Foundation under Grant DMS 0931642.

This work was also supported in part through funding from the National Institutes of Health, including Grants 1 R01 CA208253-01 (to G.B.L.), 1 R21 AI124687-01 (to G.B.L.), and 1 U01 DK108327-01 (to D.L.C. and P.A.H.) and a grant from Chi Rho Clin, Inc. (to G.B.L.).

Keywords:

  • Science & Technology
  • Multidisciplinary Sciences
  • Science & Technology - Other Topics
  • mathematical model
  • chronic pancreatitis
  • drug studies
  • TNF-ALPHA PRODUCTION
  • STELLATE CELLS
  • EXTRACELLULAR-MATRIX
  • GROWTH-FACTOR
  • LATENT TGF-BETA-1
  • ACTIVATION
  • FIBROSIS
  • CYTOKINES
  • CHEMOKINE
  • MYOFIBROBLASTS

Mathematical model of chronic pancreatitis

Tools:

Journal Title:

Proceedings of the National Academy of Sciences

Volume:

Volume 114, Number 19

Publisher:

, Pages 5011-5016

Type of Work:

Article | Final Publisher PDF

Abstract:

Chronic pancreatitis (CP) is a progressive inflammatory disease of the pancreas, leading to its fibrotic destruction. There are currently no drugs that can stop or slow the progression of the disease. The etiology of the disease is multifactorial, whereas recurrent attacks of acute pancreatitis are thought to precede the development of CP. A better understanding of the pathology of CP is needed to facilitate improved diagnosis and treatment strategies for this disease. The present paper develops a mathematical model of CP based on a dynamic network that includes macrophages, pancreatic stellate cells, and prominent cytokines that are present at high levels in the CP microenvironment. The model is represented by a system of partial differential equations. The model is used to explore in silico potential drugs that could slow the progression of the disease, for example infliximab (anti-TNF-α) and tocilizumab or siltuximab (anti-IL-6/IL-6R).

Copyright information:

© 2017 National Academy of Sciences.

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