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

Publisher: Munksgaard Country of Publication: Denmark NLM ID: 9301549 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1600-0625 (Electronic) Linking ISSN: 09066705 NLM ISO Abbreviation: Exp Dermatol Subsets: MEDLINE

Original Publication: Copenhagen : Munksgaard, c1992-

Chemotaxis, Leukocyte*; Chemokine CXCL1/*biosynthesis ; Keratinocytes/*metabolism ; Mannose-Binding Lectin/*physiology ; Neutrophils/*physiology ; Psoriasis/*immunology; Animals ; Cell Line, Transformed ; Chemokine CXCL1/genetics ; Dermis/immunology ; Dermis/pathology ; Female ; Humans ; Imiquimod/toxicity ; Inflammation ; Keratinocytes/drug effects ; Mannose-Binding Lectin/deficiency ; Mannose-Binding Lectin/genetics ; Mannose-Binding Lectin/immunology ; Mannose-Binding Lectin/pharmacology ; Metabolism, Inborn Errors/complications ; Metabolism, Inborn Errors/immunology ; Mice ; Mice, Knockout ; Psoriasis/chemically induced ; Psoriasis/metabolism ; Specific Pathogen-Free Organisms ; Up-Regulation

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.
(© 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

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2017A030313542 International Guangdong Natural Science Foundation; 81671568 International National Natural Science Foundation of China

Keywords: imiquimod; keratinocyte; mannan-binding lectin; neutrophil; psoriasis

0 (Chemokine CXCL1)
0 (Cxcl1 protein, mouse)
0 (MBL2 protein, human)
0 (Mannose-Binding Lectin)
0 (Mbl2 protein, mouse)
143107-68-0 (mannose binding protein A)
P1QW714R7M (Imiquimod)

Mannose-Binding Protein Deficiency

Date Created: 20190702 Date Completed: 20201023 Latest Revision: 20201023

20231215

10.1111/exd.13995

31260126