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Complement MASP-1 enhances adhesion between endothelial cellsand neutrophils by up-regulating E-selectin expression

Jani, Péter K. and Schwaner, Endre and Kajdácsi, Erika and Debreczeni, Márta L. and Salánki, Rita Zsanett and Dobó, József and Doleschallf, Zoltán and Rigó, János and Szabó, Bálint and Gál, Péter and Cervenak, László (2016) Complement MASP-1 enhances adhesion between endothelial cellsand neutrophils by up-regulating E-selectin expression. Molecular Immunology, 75. pp. 38-47. ISSN 0161-5890

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Abstract

The complement system and neutrophil granulocytes are indispensable in the immune response against extracellular pathogens such as bacteria and fungi. Endothelial cells also participate in antimicrobial immunity largely by regulating the homing of leukocytes through their cytokine production and their pattern of cell surface adhesion molecules. We have previously shown that mannan-binding lectin-associated serine protease-1 (MASP-1), a complement lectin pathway enzyme, is able to activate endothelial cells by cleaving protease activated receptors, which leads to cytokine production and enables neutrophil chemotaxis. Therefore, we aimed to investigate how recombinant MASP-1 (rMASP-1) can modify the pattern of P-selectin, E-selectin, ICAM-1, ICAM-2, and VCAM-1 adhesion molecules in human umbilical vein endothelial cells (HUVEC), and whether these changes can enhance the adherence between endothelial cells and neutrophil granulocyte model cells (differentiated PLB-985). We found that HUVECs activated by rMASP-1 decreased the expression of ICAM-2 and increased that of E-selectin, whereas ICAM-1, VCAM-1 and P-selectin expression remained unchanged. Furthermore, these changes resulted in increased adherence between differentiated PLB-985 cells and endothelial cells. Our finding suggests that complement MASP-1 can increase adhesion between neutrophils and endothelial cells in a direct fashion. This is in agreement with our previous finding that MASP-1 increases the production of pro-inflammatory cytokines (such as IL-6 and IL-8) and chemotaxis, and may thereby boost neutrophil functions. This newly described cooperation between complement lectin pathway and neutrophils via endothelial cells may be an effective tool to enhance the antimicrobial immune response.

Item Type: Article
Subjects: Q Science / természettudomány > QR Microbiology / mikrobiológia > QR180 Immunology / immunológia
SWORD Depositor: MTMT SWORD
Depositing User: MTMT SWORD
Date Deposited: 10 Jun 2016 09:11
Last Modified: 10 Jun 2016 09:11
URI: http://real.mtak.hu/id/eprint/36227

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