Macrophage Subset Expressing CD169 in Peritoneal Cavity-Regulated Mucosal Inflammation Together with Lower Levels of CCL
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ORIGINAL ARTICLE
Macrophage Subset Expressing CD169 in Peritoneal Cavity-Regulated Mucosal Inflammation Together with Lower Levels of CCL22 Dan Wang,1 Qiuting Li,1 Yang Yang,1 Shengyu Hao,1 Xiaolei Han,1 Jia Song,1 Yue Yin,1 Xiangzhi Li,1 Masato Tanaka,2 and Chun-Hong Qiu1,3
Abstract—Crohn’s disease (CD) and ulcerative colitis (UC) are the most widely known types of inflammatory bowel diseases (IBD) and have been paid more attention due to their increasing incidence and a substantial increase in the risk of colorectal cancer (CRC). However, the phenotype and, more importantly, the function in the regulation of mucosal inflammation by different macrophages are poorly understood, even though macrophages constitute a major subset of intestinal myeloid cells. The results firstly showed that the subset of peritoneal CD11b+CD169+ macrophages increased and CCL22 expression level decreased significantly during the DSSinduced colitis. DSS-induced colitis was alleviated in CD169-DTR mice at least partially due to the deletion CD169+ macrophages. Moreover, the CCL22 expression level in peritoneal macrophages from CD169-DTR mice was much higher than that from WT mice with DSSinduced colitis. And, the cell-sorting result revealed that CD11b+CD169+ macrophage cells did not express CCL22 dominantly. Further experiment in vivo demonstrated that treatment with recombinant murine CCL22 (rmCCL22) ameliorated the clinical symptoms of DSS-induced colitis. All these data indicated that macrophage subset of CD11b+CD169+ from peritoneal cavity played critical role probably together with low levels of CCL22 in DSS-induced colitis. KEY WORDS: peritoneal CD169+ macrophages; DSS; colitis; CCL22.
INTRODUCTION Electronic supplementary material The online version of this article (doi:10.1007/s10753-017-0562-0) contains supplementary material, which is available to authorized users. 1
Department of Cell biology, Shandong University School of Medicine, 44 Wenhua Xi Road, Jinan, 250012, Shandong, People’s Republic of China 2 Laboratory of Immune regulation, School of Life Science, Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo, 192-0392, Japan 3 To whom correspondence should be addressed at Department of Cell biology, Shandong University School of Medicine, 44 Wenhua Xi Road, Jinan, 250012, Shandong, People’s Republic of China. E-mail: [email protected] Abbreviations: CD169, Cluster of differentiation 169; CCL22, C-C motif chemokine 22; DSS, Dextran sulfate sodium; DT, Diphtheria toxin; DTR, Diphtheria toxin receptor; Tregs, Regulatory T cells; UC, Ulcerative colitis; IBD, Inflammatory bowel diseases.
Crohn’s disease (CD) and ulcerative colitis (UC) are the most widely known types of inflammatory bowel diseases (IBD) which are characterized by chronic inflammation of the gastrointestinal tract and have been the focus of attention due to their increasing incidence [1, 2]. The correlation between inflammation and the development of cancer has been confirmed by many studies, and IBD is also related to a substa
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