TY - JOUR
T1 - Mathematical model of chronic pancreatitis
AU - Hao, Wenrui
AU - Komar, Hannah M.
AU - Hart, Phil A.
AU - Conwell, Darwin L.
AU - Lesinski, Gregory B.
AU - Friedman, Avner
N1 - Funding Information:
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.).
PY - 2017/5/9
Y1 - 2017/5/9
N2 - 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).
AB - 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).
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U2 - 10.1073/pnas.1620264114
DO - 10.1073/pnas.1620264114
M3 - Article
C2 - 28439020
AN - SCOPUS:85019067777
SN - 0027-8424
VL - 114
SP - 5011
EP - 5016
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
IS - 19
ER -