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

Péter K. Jani, Endre Schwaner, Erika Kajdácsi, Márta L. Debreczeni, Rita Ungai-Salánki, J. Dobó, Zoltán Doleschall, J. Rigó, M. Geiszt, B. Szabó, P. Gál, L. Cervenák

Research output: Contribution to journalArticle

11 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)38-47
Number of pages10
JournalMolecular Immunology
Volume75
DOIs
Publication statusPublished - Jul 1 2016

Fingerprint

Mannose-Binding Protein-Associated Serine Proteases
E-Selectin
Neutrophils
Endothelial Cells
Mannose-Binding Lectin Complement Pathway
P-Selectin
Vascular Cell Adhesion Molecule-1
Chemotaxis
Intercellular Adhesion Molecule-1
Cytokines
Granulocytes
Proteinase-Activated Receptors
Human Umbilical Vein Endothelial Cells
Cell Adhesion Molecules
Interleukin-8
Immunity
Interleukin-6
Leukocytes
Fungi
Bacteria

Keywords

  • Adhesion
  • Complement
  • Endothelial cell
  • Inflammation
  • MASP-1
  • Neutrophil

ASJC Scopus subject areas

  • Molecular Biology
  • Immunology

Cite this

Complement MASP-1 enhances adhesion between endothelial cells and neutrophils by up-regulating E-selectin expression. / Jani, Péter K.; Schwaner, Endre; Kajdácsi, Erika; Debreczeni, Márta L.; Ungai-Salánki, Rita; Dobó, J.; Doleschall, Zoltán; Rigó, J.; Geiszt, M.; Szabó, B.; Gál, P.; Cervenák, L.

In: Molecular Immunology, Vol. 75, 01.07.2016, p. 38-47.

Research output: Contribution to journalArticle

Jani, Péter K. ; Schwaner, Endre ; Kajdácsi, Erika ; Debreczeni, Márta L. ; Ungai-Salánki, Rita ; Dobó, J. ; Doleschall, Zoltán ; Rigó, J. ; Geiszt, M. ; Szabó, B. ; Gál, P. ; Cervenák, L. / Complement MASP-1 enhances adhesion between endothelial cells and neutrophils by up-regulating E-selectin expression. In: Molecular Immunology. 2016 ; Vol. 75. pp. 38-47.
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AU - Debreczeni, Márta L.

AU - Ungai-Salánki, Rita

AU - Dobó, J.

AU - Doleschall, Zoltán

AU - Rigó, J.

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