Roles of chemokines in pancreatitis: A review

doi:10.4291/wjgp.v16.i4.111550

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Dec 22, 2025 (publication date) through Feb 27, 2026

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World Journal of Gastrointestinal Pathophysiology

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2150-5330

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Gastrointest Pathophysiol. Dec 22, 2025; 16(4): 111550
Published online Dec 22, 2025. doi: 10.4291/wjgp.v16.i4.111550

Roles of chemokines in pancreatitis: A review

Wei-Fang Ni, Chao-Chao Qin

Wei-Fang Ni, Chao-Chao Qin, Oncology Internal Medicine Treatment Unit, Guangyuan Traditional Chinese Medicine Hospital Affiliated to Chengdu University of Traditional Chinese Medicine, Guangyuan 628000, Sichuan Province, China

Author contributions: Ni WF and Qin CC were equal contributors to the manuscript, wrote the article.

Supported by Sichuan Provincial Geriatric Health Development Center and the Sichuan Gerontological Society, No. 24SCLN0138.

Conflict-of-interest statement: The authors declare no conflicts of interest for this article.

Corresponding author: Chao-Chao Qin, MD, PhD, Oncology Internal Medicine Treatment Unit, Guangyuan Traditional Chinese Medicine Hospital Affiliated to Chengdu University of Traditional Chinese Medicine, No. 133 Jianshe Road, Lizhou District, Guangyuan 628000, Sichuan Province, China. qinchaonannong@163.com

Received: July 3, 2025
Revised: September 1, 2025
Accepted: October 21, 2025
Published online: December 22, 2025
Processing time: 172 Days and 22.2 Hours

Core Tip

Core Tip: This review highlights the pivotal roles of chemokines in the pathogenesis of various types of pancreatitis, including acute, chronic, autoimmune, and pancreatic cancer. Chemokines like CCL2/MCP-1 and CXCL2 exacerbate acute pancreatitis by promoting neutrophil infiltration, whereas CXCL10 and CXCR3 contribute to chronic inflammation and fibrosis. CCL1-CCR8 interaction is critical for lymphocytic recruitment in autoimmune pancreatitis. Understanding the specific functions of these chemokines may lead to the development of novel therapeutic strategies targeting these inflammatory mediators.