1887

Abstract

Galectin-3 (Gal-3) is a β-galactoside lectin that is upregulated and rapidly secreted by gastric epithelial cells in response to infection. An earlier study reported the involvement of cytotoxin-associated gene A () in the expression of intracellular Gal-3. However, the role of extracellular Gal-3 and its functional significance in -infected cells remains uncharacterized. Data presented here demonstrate secretion of Gal-3 is an initial host response event in gastric epithelial cells during infection and is independent of CagA. Previously, Gal-3 was shown to bind to LPS. The present study elaborates the significance of this binding, as extracellular recombinant Gal-3 (rGal-3) was shown to inhibit the adhesion of to the gastric epithelial cells. Interestingly, a decrease in adhesion to host cells also resulted in a decrease in apoptosis. Furthermore, the study also demonstrated a chemoattractant role of extracellular rGal-3 in the recruitment of THP-1 monocytes. This study outlines the previously unidentified roles of extracellular Gal-3 where it acts as a negative regulator of adhesion and apoptosis in gastric epithelial cells, and as a chemoattractant to THP-1 monocytes. Our findings could contribute to the better understanding of how Gal-3 acts as a modulator under -induced pathological conditions.

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2016-08-01
2024-04-18
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