The regulation of inflammation by galectin-3

Authors


Tariq Sethi
Centre for Inflammation Research
The Queen’s Medical Research Institute
University of Edinburgh
49 Little France Crescent
Edinburgh, EH16 4TJ, UK
Tel.: + 44 131 242 6550
Fax: + 44 131 242 6559
e-mail: t.sethi@ed.ac.uk

Abstract

Summary:  Galectin-3 is a β-galactoside-binding animal lectin of appro- ximately 30 kDa and is evolutionarily highly conserved. Galectin-3 is promiscuous, its localization within the tissue micro-environment may be extracellular, cytoplasmic, or nuclear, and it has a concentration-dependent ability to be monomeric or form oligomers. These properties impart great flexibility on galectin-3 as a specific regulator of many biological systems including inflammation. For example, in acute tissue damage galectin-3 is a key component in the host defense against microbes such as Streptococcus pneumoniae. However, if tissue injury becomes repetitive galectin-3 also appears to be intimately involved in the transition to chronic inflammation, facilitating the walling off of tissue injury with fibrogenesis and organ scarring. Therefore galectin-3 can be viewed as a regulatory molecule acting at various stages along the continuum from acute inflammation to chronic inflammation and tissue fibrogenesis. In this review, we examine the role of galectin-3 in inflammation, and discuss the manipulation of galectin-3 expression as a potentially novel therapeutic strategy in the treatment of a broad range of inflammatory diseases.

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