Abstract
Inflammatory and fibrotic events that drive chronic pancreatitis (CP) are likely orchestrated via signaling of soluble cytokines and chemokines systemically and within the pancreas. However, a comprehensive summary of the expression of such factors during CP has not been reported to date. This information is important given continued interest in targeting cytokines that influence CP pathogenesis. Reported data on the expression change of soluble immunomodulatory factors in human CP patients were identified via a literature search using a single search term. Thirty-one articles meeting the prespecified inclusion criteria were identified to generate a compiled data summary. Compiled data demonstrated up-regulation of several factors in the blood or pancreas microenvironment of CP patients. Nine factors were elevated in both compartments, including fractalkine, IFN-γ, interleukin 1β, IL-6, IL-8, macrophage inhibitory cytokine 1, neutrophil gelatinase-associated lipocalin, transforming growth factor β, and tumor necrosis factor α. Most up-regulated factors could be classified into one of several functional groups, including inflammation, chemotaxis, angiogenesis, bone remodeling, extracellular matrix remodeling, and pain. After further validation, these factors may be used as biomarkers for disease diagnosis and identification of comorbidities, or as potential therapeutic targets.
Original language | English |
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Pages (from-to) | 986-993 |
Number of pages | 8 |
Journal | Pancreas |
Volume | 46 |
Issue number | 8 |
DOIs | |
State | Published - Sep 1 2017 |
Bibliographical note
Funding Information:From the *Comprehensive Cancer Center, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute; †Division of Gastroenterology, Hepatology, and Nutrition; ‡Comprehensive Cancer Center, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute and the Division of Gastroenterology, Hepatology, and Nutrition; §Division of Gastroenterology, Hepatology, and Nutrition, The Ohio State University Wexner Medical Center, Columbus, OH; and ||Department of Hematology and Oncology, Winship Cancer Institute of Emory University, Atlanta, GA. Received for publication October 17, 2016; accepted July 10, 2017. Address correspondence to: Gregory B. Lesinski, PhD, MPH, Department of Hematology and Oncology, Winship Cancer Institute of Emory University, Building C, Room C3090, 1365 Clifton Rd NE, Atlanta, GA 30322 (e‐mail: gregory.b.lesinski@emory.edu). The authors have no conflict of interest related to the work described in this article. This work was supported by the National Pancreas Foundation (Lesinski), the National Institutes of Health (NIH; 1R21AI124687-01; Lesinski), NIH/National Institute of Diabetes and Digestive and Kidney Diseases (1 U01 DK108327-01; Conwell and Hart), and Division of Gastroenterology, Hepatology and Nutrition at The Ohio State University. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved. DOI: 10.1097/MPA.0000000000000896
Publisher Copyright:
© 2017 Wolters Kluwer Health, Inc. All rights reserved.
Keywords
- chemokines
- chronic pancreatitis
- cytokines
- immunity
- pancreatic juice
- serum
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism
- Hepatology
- Endocrinology