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. 2007 Jan;56(1):43-51.
doi: 10.1136/gut.2005.081646. Epub 2006 May 18.

Soluble galectin-3 is a strong, colonic epithelial-cell-derived, lamina propria fibroblast-stimulating factor

E Lippert  1 , W Falk, F Bataille, T Kaehne, M Naumann, M Goeke, H Herfarth, J Schoelmerich, G Rogler
Affiliations

Soluble galectin-3 is a strong, colonic epithelial-cell-derived, lamina propria fibroblast-stimulating factor

E Lippert et al. Gut. 2007 Jan.

Abstract

Background: Colonic lamina propria fibroblasts (CLPFs) play an important role in the pathogenesis of fibrosis and strictures in Crohn's disease.

Aim: To identify colonic epithelial cell (CEC)-derived factors that activate CLPFs.

Methods: Primary human CECs and CLPFs were isolated from control mucosa and interleukin 8 (IL8) of CLPF cultures was quantified by ELISA. Activation of nuclear factor kappaB (NF-kappaB) was shown, and translocation of NF-kappaB was inhibited by a dominant-negative IkappaB-expressing adenovirus. The major CLPF-activating and IL8 inducing protein was purified using fast-performance liquid chromatography (HiPrep 16/60 Sephacryl S-200 High Resolution Column) and sodium dodecyl sulphate gel electrophoresis.

Results: A considerable increase in IL8 secretion by CLPFs cultured in CEC-conditioned media compared with that in unconditioned media (155.00 (10.00) pg/microg v 1.434 (0.695) pg/microg) was found. The effect of CEC-conditioned media on CLPF IL8 secretion was NF-kappaB dependent. A protein or DNA array confirmed the involvement of NF-kappaB and activator protein-1. Purification of a candidate band isolated with the use of sodium dodecyl sulphate-polyacrylamide gel electrophoresis and subsequent sequencing showed soluble galectin-3 to be a strong CLPF-activating factor. Depletion of galectin-3 from conditioned media by immunoprecipitation abolished the CLPF stimulatory effect.

Conclusions: Using a classical biochemical approach, soluble galectin-3 was identified as a strong activator of CLPFs produced by CEC. Galectin-3 induced NF-kappaB activation and IL8 secretion in these cells and may be a target for future therapeutic approaches to reduce or avoid stricture formation.

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Conflict of interest statement

Competing interests: None declared.

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