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ELR positive CXCL chemokines are highly expressed in an animal model of ulcerative colitis

Authors Boshagh MA, Foroutan P, Moloudi MR, Fakhari S, Malakouti P, Nikkhoo B, Jalili A

Received 1 February 2019

Accepted for publication 16 May 2019

Published 25 June 2019 Volume 2019:12 Pages 167—174

DOI https://doi.org/10.2147/JIR.S203714

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Melinda Thomas

Peer reviewer comments 2

Editor who approved publication: Dr Ning Quan


Mohammad Amin Boshagh,1,2 Poorya Foroutan,1,2 Mohammad Raman Moloudi,3 Shohreh Fakhari,1 Parisa Malakouti,1 Bahram Nikkhoo,1 Ali Jalili1,2

1Cancer and Immunology Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran; 2Department of Immunology & Hematology, Faculty of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran; 3Liver and Digestive Research Center, Kurdistan University of Medical Sciences, Sanandaj, Iran

Background: The presence of neutrophil-rich inflammation in colon tissues of patients with ulcerative colitis (UC) is one of the most important histological characteristics of this disease. However, the expression of CXCL chemokines governing the infiltration of neutrophils in UC has not been well elucidated.
Materials and methods: In this experimental study, the UC model was induced in Wistar rats by administration of 2 mL 4% acetic acid into the large colon through the rectum. Animals were anesthetized after 48 hrs; their colon tissue samples were isolated for macroscopic and histopathological examinations. The expression of CXCL family was assessed by reverse transcription polymerase chain reaction (qRT-PCR) technique.
Results: Heavy infiltration of neutrophils, coagulation necrosis, and ulcers were observed in H&E staining, which pathologically proved the UC model. qRT-PCR results showed that ELR+, CXC chemokines such as CXCL6 and CXCL3 had the highest expression in the UC group, which was 49 and 28 times higher than that of the control group, respectively. In addition, other chemokines of this group including CXCL1, CXCL2, and CXCL7 had a significant increase compared to the control group (P≤0.05). However, ELR−, CXC chemokines such as CXCL4, CXCL13, and CXCL16 showed a smaller upregulation, while CXCL14 chemokine showed a significant decrease compared to the control group (P≤0.05). However, the expression of CXCL9-12 and CXCL17 did not change.
Conclusion: The results showed that the ELR+, CXC chemokines, especially CXCL6 and CXCL3, many involved in the pathogenesis of UC; therefore, CXCL6 and CXCL3 chemokines can be used as therapeutic targets for UC, although more studies using human samples are required.

Keywords: ELR+, CXC chemokines, chemokine, CXCLs, ulcerative colitis

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