Close Homolog of L1 Deficiency Exacerbated Intestinal Epithelial Barrier Function in Mouse Model of Dextran Sulfate Sodium-Induced Colitis
The cell adhesion molecule CHL1, which belongs to the immunoglobulin superfamily, functions in a variety of physiological and pathological processes, including neural development, tissue injury, and repair. We previously found that the loss of CHL1 exacerbated the dextran sulfate sodium (DSS)-induce...
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Frontiers Media S.A.
2020-11-01
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| Series: | Frontiers in Physiology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fphys.2020.584508/full |
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| author | Ying Han Ying Han Xiaomeng Wang Xiang Cheng Ming Zhao Tong Zhao Liang Guo Dan Liu Kuiwu Wu Ming Fan Ming Fan Ming Shi Lingling Zhu Lingling Zhu |
| author_facet | Ying Han Ying Han Xiaomeng Wang Xiang Cheng Ming Zhao Tong Zhao Liang Guo Dan Liu Kuiwu Wu Ming Fan Ming Fan Ming Shi Lingling Zhu Lingling Zhu |
| author_sort | Ying Han |
| collection | DOAJ |
| description | The cell adhesion molecule CHL1, which belongs to the immunoglobulin superfamily, functions in a variety of physiological and pathological processes, including neural development, tissue injury, and repair. We previously found that the loss of CHL1 exacerbated the dextran sulfate sodium (DSS)-induced colitis in mice. In the present study, we further addressed the role of CHL1 in mouse model of DSS-induced colitis and its’ potential mechanism. Colon tissues were collected from CHL1+/+, CHL1+/−, and CHL1−/− mice after DSS induction to investigate the effects of CHL1 on the development of colitis. The data showed that CHL1 was expressed in intestine tissue, and expression of CHL1 was increased by DSS-induced inflammation. CHL1 deficiency induced more pronounced colitis features, exacerbated inflammation, and damage to colonic tissues in DSS-induced mice. Moreover, colonic tissues of CHL1−/− mice showed a marked increase in neutrophil and macrophage infiltration, be accompanied by more severe damage to intestinal epithelial cells and higher fluorescein isothiocyanate (FITC) leakage. Our results revealed deficiency of CHL1 exacerbated DSS-induced colitis, and this pathogenesis was potentially mediated by disruption of intestinal barrier integrity, indicating that CHL1 may be an attractive therapeutic target for inflammatory bowel diseases (IBDs) in mice. |
| first_indexed | 2024-12-13T05:34:06Z |
| format | Article |
| id | doaj.art-c4feb53a8268403cbf8f1dba29242131 |
| institution | Directory Open Access Journal |
| issn | 1664-042X |
| language | English |
| last_indexed | 2024-12-13T05:34:06Z |
| publishDate | 2020-11-01 |
| publisher | Frontiers Media S.A. |
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| series | Frontiers in Physiology |
| spelling | doaj.art-c4feb53a8268403cbf8f1dba292421312022-12-21T23:57:59ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2020-11-011110.3389/fphys.2020.584508584508Close Homolog of L1 Deficiency Exacerbated Intestinal Epithelial Barrier Function in Mouse Model of Dextran Sulfate Sodium-Induced ColitisYing Han0Ying Han1Xiaomeng Wang2Xiang Cheng3Ming Zhao4Tong Zhao5Liang Guo6Dan Liu7Kuiwu Wu8Ming Fan9Ming Fan10Ming Shi11Lingling Zhu12Lingling Zhu13Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, ChinaInstitute of Military Cognition and Brain Sciences, Academy of Military Medical Sciences, Beijing, ChinaInstitute of Military Cognition and Brain Sciences, Academy of Military Medical Sciences, Beijing, ChinaInstitute of Military Cognition and Brain Sciences, Academy of Military Medical Sciences, Beijing, ChinaInstitute of Military Cognition and Brain Sciences, Academy of Military Medical Sciences, Beijing, ChinaInstitute of Military Cognition and Brain Sciences, Academy of Military Medical Sciences, Beijing, ChinaInstitute of Military Cognition and Brain Sciences, Academy of Military Medical Sciences, Beijing, ChinaJiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, ChinaInstitute of Military Cognition and Brain Sciences, Academy of Military Medical Sciences, Beijing, ChinaBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, ChinaInstitute of Military Cognition and Brain Sciences, Academy of Military Medical Sciences, Beijing, ChinaJiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, ChinaInstitute of Military Cognition and Brain Sciences, Academy of Military Medical Sciences, Beijing, ChinaCo-innovation Center of Neuroregeneration, Nantong University, Nantong, ChinaThe cell adhesion molecule CHL1, which belongs to the immunoglobulin superfamily, functions in a variety of physiological and pathological processes, including neural development, tissue injury, and repair. We previously found that the loss of CHL1 exacerbated the dextran sulfate sodium (DSS)-induced colitis in mice. In the present study, we further addressed the role of CHL1 in mouse model of DSS-induced colitis and its’ potential mechanism. Colon tissues were collected from CHL1+/+, CHL1+/−, and CHL1−/− mice after DSS induction to investigate the effects of CHL1 on the development of colitis. The data showed that CHL1 was expressed in intestine tissue, and expression of CHL1 was increased by DSS-induced inflammation. CHL1 deficiency induced more pronounced colitis features, exacerbated inflammation, and damage to colonic tissues in DSS-induced mice. Moreover, colonic tissues of CHL1−/− mice showed a marked increase in neutrophil and macrophage infiltration, be accompanied by more severe damage to intestinal epithelial cells and higher fluorescein isothiocyanate (FITC) leakage. Our results revealed deficiency of CHL1 exacerbated DSS-induced colitis, and this pathogenesis was potentially mediated by disruption of intestinal barrier integrity, indicating that CHL1 may be an attractive therapeutic target for inflammatory bowel diseases (IBDs) in mice.https://www.frontiersin.org/articles/10.3389/fphys.2020.584508/fullCHL1dextran sulfate sodium (DSS)colitisintestinal barrierneutrophilmacrophage |
| spellingShingle | Ying Han Ying Han Xiaomeng Wang Xiang Cheng Ming Zhao Tong Zhao Liang Guo Dan Liu Kuiwu Wu Ming Fan Ming Fan Ming Shi Lingling Zhu Lingling Zhu Close Homolog of L1 Deficiency Exacerbated Intestinal Epithelial Barrier Function in Mouse Model of Dextran Sulfate Sodium-Induced Colitis Frontiers in Physiology CHL1 dextran sulfate sodium (DSS) colitis intestinal barrier neutrophil macrophage |
| title | Close Homolog of L1 Deficiency Exacerbated Intestinal Epithelial Barrier Function in Mouse Model of Dextran Sulfate Sodium-Induced Colitis |
| title_full | Close Homolog of L1 Deficiency Exacerbated Intestinal Epithelial Barrier Function in Mouse Model of Dextran Sulfate Sodium-Induced Colitis |
| title_fullStr | Close Homolog of L1 Deficiency Exacerbated Intestinal Epithelial Barrier Function in Mouse Model of Dextran Sulfate Sodium-Induced Colitis |
| title_full_unstemmed | Close Homolog of L1 Deficiency Exacerbated Intestinal Epithelial Barrier Function in Mouse Model of Dextran Sulfate Sodium-Induced Colitis |
| title_short | Close Homolog of L1 Deficiency Exacerbated Intestinal Epithelial Barrier Function in Mouse Model of Dextran Sulfate Sodium-Induced Colitis |
| title_sort | close homolog of l1 deficiency exacerbated intestinal epithelial barrier function in mouse model of dextran sulfate sodium induced colitis |
| topic | CHL1 dextran sulfate sodium (DSS) colitis intestinal barrier neutrophil macrophage |
| url | https://www.frontiersin.org/articles/10.3389/fphys.2020.584508/full |
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