Volume 28, Issue 9 pp. 1017-1024
ORIGINAL ARTICLE

Mannan-binding lectin promotes keratinocyte to produce CXCL1 and enhances neutrophil infiltration at the early stages of psoriasis

Jiaqi Zeng

Jiaqi Zeng

Department of Dermatology, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, China

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Xi Chen

Xi Chen

School of Laboratory Medicine and Biotechnology, Institute of Molecular Immunology, Southern Medical University, Guangzhou, China

School of Basic Medical Sciences, Department of Immunology, Southern Medical University, Guangzhou, China

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Ke Lei

Ke Lei

Department of Dermatology, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, China

School of Laboratory Medicine and Biotechnology, Institute of Molecular Immunology, Southern Medical University, Guangzhou, China

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Di Wang

Di Wang

Department of Dermatology, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, China

School of Laboratory Medicine and Biotechnology, Institute of Molecular Immunology, Southern Medical University, Guangzhou, China

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Lin Lin

Lin Lin

Department of Dermatology, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, China

School of Basic Medical Sciences, Department of Immunology, Southern Medical University, Guangzhou, China

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Yajie Wang

Yajie Wang

Department of Dermatology, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, China

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Yao Li

Yao Li

Department of Dermatology, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, China

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Yunzhi Liu

Yunzhi Liu

School of Laboratory Medicine and Biotechnology, Institute of Molecular Immunology, Southern Medical University, Guangzhou, China

School of Basic Medical Sciences, Department of Immunology, Southern Medical University, Guangzhou, China

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Liyun Zhang

Liyun Zhang

School of Basic Medical Sciences, Department of Immunology, Southern Medical University, Guangzhou, China

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Daming Zuo

Corresponding Author

Daming Zuo

School of Laboratory Medicine and Biotechnology, Institute of Molecular Immunology, Southern Medical University, Guangzhou, China

School of Basic Medical Sciences, Department of Immunology, Southern Medical University, Guangzhou, China

Guangdong Provincial Key Laboratory of Proteomics, Southern Medical University, Guangzhou, China

Correspondence

Ledong Sun, Department of Dermatology, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, 510900, China.

Email: [email protected]

Daming Zuo, School of Laboratory Medicine and Biotechnology, Institute of Molecular Immunology, Southern Medical University, Guangzhou, 510515, China.

Email: [email protected]

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Ledong Sun

Corresponding Author

Ledong Sun

Department of Dermatology, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, China

Correspondence

Ledong Sun, Department of Dermatology, The Fifth Affiliated Hospital, Southern Medical University, Guangzhou, 510900, China.

Email: [email protected]

Daming Zuo, School of Laboratory Medicine and Biotechnology, Institute of Molecular Immunology, Southern Medical University, Guangzhou, 510515, China.

Email: [email protected]

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First published: 01 July 2019
Citations: 14
Jiaqi Zeng and Xi Chen contributed equally to this work.

Funding information

This work was supported in part by National Natural Science Foundation of China 81671568 and Guangdong Natural Science Foundation 2017A030313542.

Abstract

Psoriasis is a chronic, relapsing inflammatory skin disorder. Numerous experimental evidence and therapeutic evidence have shown that the innate immune response is critical for the pathogenesis and development of psoriasis. Mannan-binding lectin (MBL), a prototypic pattern recognition molecule of the innate immune system, plays an essential role in the host defense against certain infections and also appears to be a major regulator of inflammation. In this study, we investigated the function of MBL on the course of experimental murine imiquimod (IMQ)-induced psoriasis. Our data showed that MBL-deficient (MBL−/−) mice exhibited attenuated skin damage characterized by greatly decreased erythema compared with wild-type control mice during the early stages of IMQ-induced psoriasis-like skin inflammation. The reduced skin inflammation in MBL−/− mice was associated with the decreased infiltration of neutrophils. Furthermore, we have determined that MBL deficiency limited the chemokine CXCL1 production from skin keratinocytes upon IMQ stimulation, which might be responsible for the impaired skin recruitment of neutrophils. Additionally, we have provided the data that MBL protein promotes the IMQ-induced expression of CXCL1 and activation of MAPK/NF-κB signalling pathway in human keratinocyte HaCaT cells in vitro. In summary, our study revealed an unexpected role of MBL on keratinocyte function in skin, thus offering a new insight into the pathogenic mechanisms of psoriasis.

CONFLICT OF INTEREST

The authors have no conflict of interest to declare.

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