Galactin-1, 3 and 9: Potential biomarkers in idiopathic pulmonary fibrosis and other interstitial lung diseases

d’Alessandro, Miriana; Vita, Elda De; Bergantini, Laura; Mazzei, Maria Antonietta; Valvasone, S Di; Bonizzoli, Manuela; Peris, Adriano; Sestini, Piersante; Bargagli, Elena; Bennett, David

doi:10.1016/j.resp.2020.103546

Cited by 24 publications

(10 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Germano et al reported that Prominin-1/CD133+ lung epithelial progenitors protected against bleomycin-induced pulmonary fibrosis [ 50 ]. In our study, we observed higher expression of CD133/1 in IPF patients than in controls: this result probably reflects the compensation of the profibrotic/antifibrotic protein imbalance typical of IPF [ 51 , 52 , 53 , 54 , 55 , 56 , 57 ].…”

Section: Discussionsupporting

confidence: 55%

Extracellular Vesicle Surface Signatures in IPF Patients: A Multiplex Bead-Based Flow Cytometry Approach

d’Alessandro

Soccio

Bergantini

et al. 2021

Cells

Self Cite

View full text Add to dashboard Cite

Background: Extracellular vesicles (EVs) are secreted by cells from their membrane within circulation and body fluids. Knowledge of the involvement of EVs in pathogenesis of lung diseases is increasing. The present study aimed to evaluate the expression of exosomal surface epitopes in a cohort of idiopathic pulmonary fibrosis (IPF) patients followed in two Italian Referral Centres for Interstitial Lung Diseases, comparing them with a group of healthy volunteers. Materials and Methods: Ninety IPF patients (median age and interquartile range (IQR) 71 (66–75) years; 69 males) were selected retrospectively. Blood samples were obtained from patients before starting antifibrotic therapy. A MACSPlex Exosome Kit, human, (Miltenyi Biotec, Bergisch-Gladbach, Germany), to detect 37 exosomal surface epitopes, was used. Results: CD19, CD69, CD8, and CD86 were significantly higher in IPF patients than in controls (p = 0.0023, p = 0.0471, p = 0.0082, and p = 0.0143, respectively). CD42a was lower in IPF subjects than in controls (p = 0.0153), while CD209, Cd133/1, MCSP, and ROR1 were higher in IPF patients than in controls (p = 0.0007, p = 0.0050, p = 0.0139, and p = 0.0335, respectively). Kaplan–Meier survival analysis for IPF patients: for median values and a cut-off of 0.48 for CD25, the two subgroups showed a significant difference in survival rate (p = 0.0243, hazard ratio: 0.52 (95%CI 0.29–0.92); the same was true for CD8 (cut-off 1.53, p = 0.0309, hazard ratio: 1.39 (95%CI 0.75–2.53). Conclusion: Our multicenter study showed for the first time the expression of surface epitopes on EVs from IPF patients, providing interesting data on the communication signatures/exosomal profile in serum from IPF patients and new insights into the pathogenesis of the disease and a promising reliability in predicting mid-term survival of IPF patients.

show abstract

Section: Discussionsupporting

confidence: 55%

Extracellular Vesicle Surface Signatures in IPF Patients: A Multiplex Bead-Based Flow Cytometry Approach

d’Alessandro

Soccio

Bergantini

et al. 2021

Cells

Self Cite

View full text Add to dashboard Cite

show abstract

“…Galectin-3 is another potential target under investigation as antifibrotic therapy in IPF. Galectin-3 is a pro-fibrotic ß-galactoside-binding lectin implicated in the pathogenesis of IPF and IPF exacerbations [ 55 , 56 ]. A phase 1/2a study with Td139, an inhaled inhibitor of galectin-3, in healthy subjects and patients with IPF has provided promising results [ 56 ].…”

Section: Treatment Of Progressive Fibrosing Interstitial Lung Diseasementioning

confidence: 99%

Progressive Fibrosing Interstitial Lung Diseases: A Current Perspective

et al. 2021

View full text Add to dashboard Cite

Interstitial lung diseases (ILDs) are a large and diverse group of rare and chronic respiratory disorders, with idiopathic pulmonary fibrosis (IPF) being the most common and best-studied member. Increasing interest in fibrosis as a therapeutic target and the appreciation that fibrotic mechanisms may be a treatable target of IPF prompted the development and subsequent approval of the antifibrotics, pirfenidone and nintedanib. The management of ILDs has changed considerably following an understanding that IPF and some ILDs share similar disease behavior of progressive fibrosis, termed “progressive fibrosing phenotype”. Indeed, antifibrotic treatment has shown to be beneficial in ILDs characterized by the progressive fibrosing phenotype. This narrative review summarizes current knowledge in the field of progressive fibrosing ILDs. Here, we discuss the clinical characteristics and pathogenesis of lung fibrosis and highlight relevant literature concerning the mechanisms underlying progressive fibrosing ILDs. We also summarize current diagnostic approaches and the available treatments of progressive fibrosing ILDs and address the optimization of treating progressive fibrosing ILDs with antifibrotics in clinical practice.

show abstract

“…These cell-cell and cell-matrix interactions, as well as signalling pathways on the cell surface, influence and modulate cell functions, such as inflammatory and immune responses [9]. Depending on the type of inflammatory stimulus, the microenvironment and the target cells involved, these proteins may be associated with pro-or anti-inflammatory responses [10]. Galectins are also implicated in pulmonary fibrosis, where their inhibition may be useful in therapeutic management [11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

“…Depending on the type of inflammatory stimulus, the microenvironment and the target cells involved, these proteins may be associated with pro- or anti-inflammatory responses [ 10 ]. Galectins are also implicated in pulmonary fibrosis, where their inhibition may be useful in therapeutic management [ 11 – 14 ]. Some reports show that malignant transformation in human cancer patients is often associated with altered galectin expression [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

“…Some reports show that malignant transformation in human cancer patients is often associated with altered galectin expression [ 15 ]. Galectins play a crucial role in the homeostasis of inflammation through their apoptotic effect on activated leukocytes [ 11 , 16 ]. Release of Gals-1 and 3 initiates an inflammatory response in several ways, including binding of neutrophils to the endothelium, trafficking of neutrophils through the extracellular matrix bound to laminins and fibronectin, and acting as chemotactic agents towards the site of inflammation [ 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The Role of Galectins in Chronic Lung Allograft Dysfunction

d’Alessandro

Bergantini

Fossi

et al. 2021

Lung

Self Cite

View full text Add to dashboard Cite

Background Galectins are proteins that bind β-galactosides such as N-acetyllactosamine present in N-linked and O-linked glycoproteins and that seem to be implicated in inflammatory and immune responses as well as fibrotic mechanisms. This preliminary study investigated serum galectins as clinical biomarkers in lung transplant patients with chronic lung allograft dysfunction (CLAD), phenotype bronchiolitis obliterans syndrome (BOS). Materials and Methods Nineteen lung transplant patients [median age (IQR), 55 (45–62) years; 53% males] were enrolled in the study. Peripheral blood concentrations of galectins-1, 3 and 9 were determined with commercial ELISA kits. Results Galectin-1 concentrations were higher in BOS than in stable LTX patients (p = 0.0394). In logistic regression analysis, testing BOS group as dependent variable with Gal-1 and 3 as independent variables, area under the receiver operating characteristics (AUROC) curve was 98.9% (NPV 90% and PPV 88.9%, p = 0.0003). With the stable LTX group as dependent variable and Gal-1, 3 and 9 as independent variables, AUROC was 92.6% (NPV 100% and PPV 90%, p = 0.0023). In stable patients were observed an inverse correlation of Gal-3 with DLCO% and KCO%, and between Gal-9 and KCO%. Conclusion Galectins-1, 3 and 9 are possible clinical biomarkers in lung transplant patients with diagnostic and prognostic meaning. These molecules may be directly implicated in the pathological mechanisms of BOS. The hypothesis that they could be new therapeutic targets in BOS patients is intriguing and also worth exploring.

show abstract

Galactin-1, 3 and 9: Potential biomarkers in idiopathic pulmonary fibrosis and other interstitial lung diseases

Cited by 24 publications

References 13 publications

Extracellular Vesicle Surface Signatures in IPF Patients: A Multiplex Bead-Based Flow Cytometry Approach

Extracellular Vesicle Surface Signatures in IPF Patients: A Multiplex Bead-Based Flow Cytometry Approach

Progressive Fibrosing Interstitial Lung Diseases: A Current Perspective

The Role of Galectins in Chronic Lung Allograft Dysfunction

Contact Info

Product

Resources

About