Abstract
Galectin-3 is a β-galactoside-binding lectin implicated in the fine-tuning of innate immunity. Rhodococcus equi, a facultative intracellular bacterium of macrophages, causes severe granulomatous bronchopneumonia in young horses and immunocompromised humans. The aim of this study is to investigate the role of galectin-3 in the innate resistance mechanism against R. equi infection. The bacterial challenge of galectin-3-deficient mice (gal3-/-) and their wild-type counterpart (gal3+/+) revealed that the LD50 for the gal3-/- mice was about seven times higher than that for the gal3+/+ mice. When challenged with a sublethal dose, gal3-/- mice showed lower bacteria counts and higher production of IL-12 and IFN-γ production, besides exhibiting a delayed although increased inflammatory reaction. Gal3-/- macrophages exhibited a decreased frequency of bacterial replication and survival, and higher transcript levels of IL-1β, IL-6, IL-10, TLR2 and MyD88. R. equi-infected gal3+/+ macrophages showed decreased expression of TLR2, whereas R. equi-infected gal3-/- macrophages showed enhanced expression of this receptor. Furthermore, galectin-3 deficiency in macrophages may be responsible for the higher IL-1β serum levels detected in infected gal3-/- mice. Therefore galectin-3 may exert a regulatory role in innate immunity by diminishing IL-1β production and thus affecting resistance to R. equi infection.
Original language | English (US) |
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Pages (from-to) | 2762-2775 |
Number of pages | 14 |
Journal | European Journal of Immunology |
Volume | 38 |
Issue number | 10 |
DOIs | |
State | Published - 2008 |
Keywords
- Bacterial infections
- Galectin-3
- IL-1β
- Innate immunity
- Toll-like receptor
ASJC Scopus subject areas
- Immunology
- Immunology and Allergy