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

Area of Science:

• Immunology
• Cell Biology
• Complement System

Background:

• The complement system and neutrophils are crucial for fighting extracellular pathogens.
• Endothelial cells regulate immune cell homing via cytokines and adhesion molecules.
• Mannan-binding lectin-associated serine protease-1 (MASP-1) activates endothelial cells, promoting neutrophil chemotaxis.

Purpose of the Study:

• To investigate how recombinant MASP-1 (rMASP-1) affects adhesion molecule expression in human umbilical vein endothelial cells (HUVECs).
• To determine if rMASP-1-induced changes enhance endothelial cell adherence to neutrophil granulocytes.

Main Methods:

• Treatment of HUVECs with rMASP-1.
• Analysis of P-selectin, E-selectin, ICAM-1, ICAM-2, and VCAM-1 expression.
• Assessment of adherence between HUVECs and differentiated PLB-985 neutrophil model cells.

Main Results:

• rMASP-1 decreased ICAM-2 and increased E-selectin expression on HUVECs.
• Expression of ICAM-1, VCAM-1, and P-selectin remained unchanged.
• Enhanced adherence was observed between rMASP-1-activated HUVECs and differentiated PLB-985 cells.

Conclusions:

• Complement MASP-1 directly increases neutrophil-endothelial cell adhesion.
• This mechanism complements MASP-1's known role in cytokine production and chemotaxis.
• This interaction enhances the antimicrobial immune response via the complement lectin pathway and neutrophils.