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The effects of galectin‐3 depletion apheresis on induced skin inflammation in a porcine model
Author(s) -
NavarroAlvarez Nalu,
Goncalves Beatriz,
Andrews Alec R,
Wang Zhaohui,
Wang Zhirui,
Harrington Edward,
Shah Jigesh,
Sachs David H.,
Eliaz Isaac,
Huang Christene A.
Publication year - 2018
Publication title -
journal of clinical apheresis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.697
H-Index - 46
eISSN - 1098-1101
pISSN - 0733-2459
DOI - 10.1002/jca.21624
Subject(s) - inflammation , medicine , galectin 3 , apheresis , antibody , immunology , fibrosis , angiogenesis , pathology , cancer research , platelet
Galectin‐3 (Gal‐3), a β‐galactoside‐binding lectin that is expressed in mammalian cells, is known to modulate several biological functions such as cell‐cell adhesion, macrophage activation, angiogenesis, metastasis, and fibrosis. The goal of this study was to evaluate the ability of Gal‐3 depletion apheresis using an adsorption column with immobilized anti‐Gal‐3‐antibody to reduce inflammation induced by Complete Freund's Adjuvant injection in a skin inflammation porcine model. Here, we report that plasma perfusion by apheresis through a Gal‐3 binding immuno‐affinity column reduces plasma Gal‐3 levels to below limits of quantitative detection, and results in significant decrease in skin inflammation, including degree and duration of inflammatory lesions. Human plasma was tested ex vivo and found to be efficiently depleted using the anti‐Gal‐3 affinity column. This study demonstrates the potential of Gal‐3 depletion apheresis as a therapeutic method for inflammation‐mediated disease, supporting continued research in this area for clinical application.