Eosinophils, galectins, and a reason to breathe

Rosenberg, Helene F.; Druey, Kirk M.

doi:10.1073/pnas.1610644113

Cited by 6 publications

(8 citation statements)

References 26 publications

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“…7 Additionally, gal-9 is an eosinophilic chemo-attractant protein. 6 By these regulating functions, increased gal-9 in AD could participate in pathogenesis of AD, and its inhibition may help in improvement the diseases course in those patients. 19 Moreover, it was reported that gal-9 participates in the development of a number of allergic disorders including asthma 20,21 and food allergy.…”

Section: Discussionmentioning

confidence: 99%

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<p>Role of Galectin-9 in Atopic Dermatitis — Is It Mediated Through E Selectin? A Clinical and Immunohistochemical Study</p>

Farag

Al-Sharaky

Allam³

et al. 2020

CCID

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Background: Atopic dermatitis (AD) is a recognized T helper (Th)2, allergic, skin disease. Galectin-9 (gal-9) is a member of galectin family. It alters T-cell balance resulting in Th2 polarization. These Th2 cells yield various cytokines that may influence E selectin expression. Therefore, we hypothesized that gal-9 may have an active role in AD and this role could be mediated through E selectin. Objective: To assess this hypothesis, immunohistochemical expression of gal-9 and E selectin was investigated in skin lesions, from atopic dermatitis patients, and compared. Methods: Twenty-two atopic dermatitis patients and ten controls were included in this casecontrol study. SCORAD score was used to evaluate atopic dermatitis severity. Biopsies from skin lesions of AD patients and matched sites of controls were taken and stained immunohistochemically by gal-9 and E selectin polyclonal antibodies. Results: Compared to controls, atopic dermatitis patients exhibited a significant increased gal-9 H score, percent of expression, cellular localization (P˂0.001) and intensity (P=0.04) as well as dermal cellular infiltrate (P˂0.001). Also, there were significant elevations in E selectin H score (P=0.002), percent of expression (P=0.001) and cellular localization (P<0.001) as well as dermal inflammatory infiltrates in AD cases than controls. In AD, 20 cases showed co expression of both gal-9 and E selectin in the epidermis with insignificant correlation between their H scores. Study Limitations: This study only included a small number of studied subjects. Conclusion: Galectin-9 and E selectin participates independently in atopic dermatitis pathogenesis, that may help in development of new therapeutic agents in atopic dermatitis management program.

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Section: Discussionmentioning

confidence: 99%

“…Also, gal-9 has been well characterized as an eosinophilic chemoattractant. 6 Additionally, it modifies T-cell balance, resulting in polarization of Th2 cells. 7 Through these functions, gal-9 can alter many physiological and pathological processes including allergy.…”

Section: Introductionmentioning

confidence: 99%

<p>Role of Galectin-9 in Atopic Dermatitis — Is It Mediated Through E Selectin? A Clinical and Immunohistochemical Study</p>

Farag

Al-Sharaky

Allam³

et al. 2020

CCID

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“…In this study, we demonstrated that galectin‐13 expression is located in airway epithelial cells and submucosal gland cells. Galectins participate in the signalling pathway, gene expression and vesicular trafficking, et al 28 Several galectins, particularly galectin−3, galectin−9, and galectin −10, have been shown to play important roles in modulating allergic inflammatory responses 11 . Among them, galectin‐3 showed the capacity to bind IgE 29 .…”

Section: Discussionmentioning

confidence: 99%

“…Galectins are a family of β‐galactoside‐binding lectins that regulate diverse biological processes including cell activation, cell adhesion, migration, cell growth, phagocytosis and apoptosis 8‐10 . Fifteen members of the galectin family have been identified in humans, and galectin‐1, 3, 9, 10 are involved in eosinophilic inflammation 11 …”

Section: Introductionmentioning

confidence: 99%

Increased epithelial galectin‐13 expression associates with eosinophilic airway inflammation in asthma

Zhang

Feng

et al. 2021

Clin Experimental Allergy

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Background Airway eosinophilic inflammation is a central feature in asthma which is mainly driven by type 2 response. The expression of galectin‐13 was up‐regulated in a parasitic infection model which is also characterized by type 2 immune response. We hypothesized that galectin‐13 may be involved in airway eosinophilic inflammation in asthma. Objective To unveil the role of galectin‐13 in asthma airway inflammation. Methods We measured galectin‐13 expressions in bronchial brushings, sputum, and plasma of asthma patients (n = 54) and healthy controls (n = 15), and analysed the correlations between galectin‐13 expression and airway eosinophilia. We used human bronchial epithelial cell line 16HBE to investigate the possible mechanism by which galectin‐13 participates in eosinophilic inflammation. Results The expression of galectin‐13 was markedly increased in subjects with asthma compared to controls. Epithelial galectin‐13 mRNA levels in asthmatic subjects were strongly correlated with eosinophilic airway inflammation (the percentage of sputum eosinophils, the number of eosinophils in bronchial submucosa and FeNO) and the expression of Th2 signature genes (CLCA1, POSTN and SERPINB2). Inhaled corticosteroid (ICS) treatment reduced plasma galectin‐13 levels, and baseline plasma galectin‐13 levels reflect the response to ICS treatment. In cultured 16HBE cells, knockdown of galectin‐13 suppressed IL‐13‐stimulated MCP‐1 and eotaxin‐1 expression by inhibiting the activation of EGFR and ERK. Conclusions & Clinical Relevance Galectin‐13 is a novel marker for airway eosinophilia in asthma, and may contribute to allergic airway eosinophilic inflammation by up‐regulating the expression of MCP‐1 and eotaxin‐1. Plasma galectin‐13 levels may be useful for predicting responses to ICS treatment.

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“…Treatment with PCI significantly suppressed these protein expressions in the tissues and cells, further suggesting simultaneous but not sequential interactions existed between the two proteins. Though HDAC8 and Gal-3 have been reported as factors involved in pathological process of allergic asthma [15,[31][32][33], a combined pattern of HDAC8 interacting with Gal-3 is still unclear in asthma.…”

Section: Discussionmentioning

confidence: 99%

HDAC8 inhibitor attenuates airway responses to antigen stimulus through synchronously suppressing galectin-3 expression and reducing macrophage-2 polarization

Ren

et al. 2020

Respir Res

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Background: This study was to investigate of the mechanism by which histone deacetylase (HDAC) 8 inhibitor ameliorated airway hyperresponsiveness (AHR) and allergic airway inflammation. Methods: Mice were sensitized and then treated with budesonide (BUD) or PCI-34051 (PCI) prior to exposing to normal saline (NS) or ovalbumin (OVA). The raw264.7 cells were treated with interleukin (IL)-4 and PCI or shRNA alone. Repetitive measurements of enhanced pause (Penh) were executed by increasing concentrations of acetyl-βmethacholine chloride (0 -50 mg/ml). Cells in bronchoalveolar lavage fluid (BALF) and pathological changes of lungs were examined, respectively. The expression levels of HDAC8, Galecitn (Gal)-3, CD68, CD86, CD163, Arg1 and NOS2 in lungs were measured. Co-regulation of HDAC8 and Gal-3 proteins was observed by immunofluorescence staining and co-immunoprecipitation assay (Co-IP). Results: Significant increases in Penh and IL-4 level were detected with a large inflammatory infiltrate, comprised predominantly of macrophages and eosinophils, into the BALF in OVA-exposed lungs. HDAC8, Gal-3, CD68, CD86, CD163, Arg1 and NOS2 proteins were over-expressed with the significant changes in the Arg1 and NOS2 mRNA levels in the lungs and the IL-4-treated cells. PCI intervention obviously reduced the counts of CD163 + cells. Furthermore, Gal-3 knockdown suppressed Arg1 expression in the cells. Immunofluorescence staining displayed simultaneous changes in HDAC8 and Gal-3 expression in the investigated samples. Treatment with PCI resulted in synchronous reduction of HDAC8 and Gal-3 expression in the Co-IP complexes. Conclusions: The HDAC8 inhibitor ameliorates AHR and airway inflammation in animal model of allergic asthma through reducing HDAC8-Gal-3 interaction and M2 macrophage polarization.

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Eosinophils, galectins, and a reason to breathe

Cited by 6 publications

References 26 publications

<p>Role of Galectin-9 in Atopic Dermatitis — Is It Mediated Through E Selectin? A Clinical and Immunohistochemical Study</p>

<p>Role of Galectin-9 in Atopic Dermatitis — Is It Mediated Through E Selectin? A Clinical and Immunohistochemical Study</p>

Increased epithelial galectin‐13 expression associates with eosinophilic airway inflammation in asthma

HDAC8 inhibitor attenuates airway responses to antigen stimulus through synchronously suppressing galectin-3 expression and reducing macrophage-2 polarization

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