Data from: Protective effect of Galectin-9 in murine model of lung emphysema: involvement of neutrophil migration and MMP-9 production

Purpose: Chronic obstructive pulmonary disease (COPD) is characterized by
irreversible airflow obstruction and pulmonary emphysema. Persistent
inflammation and remodeling of the lungs and airways result in reduced
lung function and a lower quality of life. Galectin (Gal)-9 plays a
crucial role as an immune modulator in various diseases. However, its role
in the pathogenesis of pulmonary emphysema is unknown. This study
investigates whether Gal-9 is involved in pulmonary inflammation and
changes in emphysema in a porcine pancreatic elastase (PPE)-induced
emphysema model. Materials and Methods: Gal-9 was administered to mice
subcutaneously once daily from 1 day before PPE instillation to day 5.
During the development of emphysema, lung tissue and bronchoalveolar
lavage fluid (BALF) were collected. Histological and cytological findings,
concentrations of chemokines and matrix metalloproteinases (MMPs) in the
BALF, and the influence of Gal-9 treatment on neutrophils were analyzed.
Results: Gal-9 suppressed the pathological changes of PPE-induced
emphysema. The mean linear intercept (Lm) of Gal-9-treated emphysema mice
was significantly lower than that of PBS-treated emphysema mice (66.1 ±
3.3 µm vs. 118.8 ± 14.8 µm, respectively; p < 0.01). Gal-9
decreased the number of neutrophils and levels of MMP-9, MMP-2 and tissue
inhibitor of metalloproteinases (TIMP)-1 in the BALF. The number of
neutrophils in the BALF correlated significantly with MMPs levels.
Interestingly, Gal-9 pretreatment in vitro inhibited the chemotactic
activity of neutrophils and MMP-9 production from neutrophils.
Furthermore, in Gal-9-deficient mice, PPE-induced emphysema progressed
significantly compared with that in wild–type (WT) mice (108.7 ± 6.58 µm
vs. 77.19 ± 6.97 µm, respectively; p < 0.01). Conclusions: These
results suggest that Gal-9 protects PPE-induced inflammation and emphysema
by inhibiting the infiltration of neutrophils and decreasing MMPs levels.
Exogenous Gal-9 could be a potential therapeutic agent for COPD.