Galectn-3 : marker of airway inflammation in bronchial asthma

Elkolaly, Reham M.; Ali, Dareen Abdelaziz Mohammed

doi:10.1183/13993003.congress-2018.pa954

Cited by 2 publications

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“…Despite its known contribution during chronic lung disease, the role of Gal-3 in the development of acute lung injury (ALI) remains unclear. In humans, Gal-3 is a marker of airway inflammation in bronchial asthma ( Elkolaly and Ali, 2018 ) and is elevated in patients with chronic obstructive pulmonary disease (COPD), where it is associated with neutrophil accumulation in the small airways ( Pilette et al, 2007 ). It has also recently been implicated for its role in inflammatory and fibrotic responses following COVID-19 infection ( Garcia-Revilla et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Selective Myeloid Depletion of Galectin-3 Offers Protection Against Acute and Chronic Lung Injury

et al. 2021

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Rationale: Galectin-3 (Gal-3) is an immune regulator and an important driver of fibrosis in chronic lung injury, however, its role in acute lung injury (ALI) remains unknown. Previous work has shown that global deletion of galectin-3 reduces collagen deposition in a bleomycin-induced pulmonary fibrosis model (MacKinnon et al., Am. J. Respir. Crit. Care Med., 2012, 185, 537–46). An inhaled Gal-3 inhibitor, GB0139, is undergoing Phase II clinical development for idiopathic pulmonary fibrosis (IPF). This work aims to elucidate the role of Gal-3 in the myeloid and mesenchymal compartment on the development of acute and chronic lung injury.Methods:LgalS3fl/fl mice were generated and crossed with mice expressing the myeloid (LysM) and mesenchymal (Pdgfrb) cre drivers to yield LysM-cre+/-/LgalS3fl/fl and Pdgfrb-cre+/-/LgalS3fl/fl mice. The response to acute (bleomycin or LPS) or chronic (bleomycin) lung injury was compared to globally deficient Gal-3−/− mice.Results: Myeloid depletion of Gal-3 led to a significant reduction in Gal-3 expression in alveolar macrophages and neutrophils and a reduction in neutrophil recruitment into the interstitium but not into the alveolar space. The reduction in interstitial neutrophils corelated with decreased levels of pulmonary inflammation following acute bleomycin and LPS administration. In addition, myeloid deletion decreased Gal-3 levels in bronchoalveolar lavage (BAL) and reduced lung fibrosis induced by chronic bleomycin. In contrast, no differences in BAL Gal-3 levels or fibrosis were observed in Pdgfrb-cre+/-/LgalS3fl/flmice.Conclusions: Myeloid cell derived Galectin-3 drives acute and chronic lung inflammation and supports direct targeting of galectin-3 as an attractive new therapy for lung inflammation.

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Section: Introductionmentioning

confidence: 99%

Selective Myeloid Depletion of Galectin-3 Offers Protection Against Acute and Chronic Lung Injury

et al. 2021

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“…Furthermore, the great variability in the tissue raises the necessity of having more than one sample ( Diamant et al, 2019 ). Some less-invasive markers include sputum matrix metalloproteinase 2 (MMP-2), fibroblast growth factor 2 (FGF-2) and galectin-3, the latter being predictive of omalizumab effects on airway remodeling ( Mauri et al, 2014 ; Elkolaly and Ali, 2018 ; Sivakoti et al, 2018 ; Tan et al, 2020 ). Other airways remodeling markers include CCL16, released by bronchiolar exocrine cells, which is usually measured in the sputum and compared to IL-8 levels (F. Schleich et al, 2016 ).…”

Section: Biomarkers For Asthmamentioning

confidence: 99%

Latest Progresses in Allergic Diseases Biomarkers: Asthma and Atopic Dermatitis

Puzzovio

Levi‐Schaffer

2021

Front. Pharmacol.

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In the last years, the understanding of the pathologic mechanisms of asthma and atopic dermatitis, both characterized by allergic inflammation, has greatly improved. However, it is evident that both diseases present with high heterogeneity, which complicates the diagnosis and the therapeutic approach of the patients. Moreover, some of the currently available strategies to treat asthma and atopic dermatitis are still mostly controlling the symptoms, but not to lead towards full healing, thus having these two diseases labelled as unmet clinical needs by WHO. Therefore, the “one-size-fits-all” strategy is outdated for asthma and atopic dermatitis, and there is the need of better methods to clearly diagnose the disease and tailor the therapy according to the specific symptomatology. In this regard, the use of biomarkers has been advanced in order to characterize both diseases according to their clinical signs and to facilitate the subsequent treatment. Despite the advancements made in this regard, there is still need for better and more sensitive biomarkers and for less invasive sampling methodologies, with the aim to diagnose specifically each manifestation of asthma and atopic dermatitis and to provide the best treatment with the least suffering for the patients.

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Galectn-3 : marker of airway inflammation in bronchial asthma

Cited by 2 publications

References 0 publications

Selective Myeloid Depletion of Galectin-3 Offers Protection Against Acute and Chronic Lung Injury

Selective Myeloid Depletion of Galectin-3 Offers Protection Against Acute and Chronic Lung Injury

Latest Progresses in Allergic Diseases Biomarkers: Asthma and Atopic Dermatitis

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