Galectin‐3 is an amplifier of the interleukin‐1 β‐mediated inflammatory response in corneal keratinocytes
Open accessAbstract
Summary: Interleukin‐1 β (IL‐1 β) is a potent mediator of innate immunity commonly up‐regulated in a broad spectrum of inflammatory diseases. When bound to its cell surface receptor, IL‐1 β initiates a signalling cascade that cooperatively induces the expression of canonical IL‐1 target genes such as IL‐8 and IL‐6. Here, we present galectin‐3 as a novel regulator of IL‐1 β responses in corneal keratinocytes. Using the SNAP‐tag system and digitonin semi‐permeabilization, we show that recombinant exogenous galectin‐3 binds to the plasma membrane of keratinocytes and is internalized into cytoplasmic compartments. We find that exogenous galectin‐3, but not a dominant negative inhibitor of galectin‐3 polymerization lacking the N‐terminal domain, exacerbates the response to IL‐1 β by stimulating the secretion of inflammatory cytokines. The activity of galectin‐3 could be reduced by a novel d‐galactopyranoside derivative targeting the conserved galactoside‐binding site of galectins and did not involve interaction with IL‐1 receptor 1 or the induction of endogenous IL‐1 β. Consistent with these observations, we demonstrate that small interfering RNA‐mediated suppression of endogenous galectin‐3 expression is sufficient to impair the IL‐1 β‐induced secretion of IL‐8 and IL‐6 in a p38 mitogen‐activated protein kinase‐independent manner. Collectively, our findings provide a novel role for galectin‐3 as an amplifier of IL‐1 β responses during epithelial inflammation through an as yet unidentified mechanism.
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Selectin and galectin pathways promote feedforward stimulation of interleukin production.
“Vascular signaling networks demonstrated marked upregulation of pro-inflammatory selectin and galectin pathways (Fig. 7, G and H, fig. S17, C and D), which promote feedforward stimulation of interleukin production (64-66).”
From Molecular and cellular processes disrupted in the early postnatal Down syndrome prefrontal cortex (2026) · cites this paper as [64]
The Discussion (page unavailable) reports that galectin-3 increased IL-1β-induced secretion of IL-8 and IL-6 in corneal keratinocytes and speculates that it may provide positive feedback. It does not establish a selectin pathway or increased interleukin production generally; galectin-3 did not increase IL-1β levels in these cells, and its effect on IL-8 and IL-6 was on secretion rather than mRNA expression. (LLM, conf=0.87)
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- Authors
- Uchino, Y., Woodward, A. M., Mauris, J., Peterson, K., Verma, P., Nilsson, U. J., Rajaiya, J., & Argüeso, P.
- Affiliations
- Massachusetts Eye and Ear Infirmary (US)
- Lund University (SE)
- Corresponding author
- Argüeso, Pablo
- Venue
- Immunology
- Publisher
- Wiley
- Published
- 2018-02-15
- Volume
- 154
- Issue
- 3
- Pages
- 490-499
- ISSN
- 0019-2805 (ISSN-L)
- 1365-2567
- PMC
- PMC6002218
- OpenAlex
- W2791975168
- Cited by
- 31
- References
- 48
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 1 · 2023: 2 · 2022: 3 · 2021: 6 · 2020: 7 · 2019: 1 · 2018: 2
- FWCI
- 1.72
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Immunology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- National Institutes of Health
- National Eye Institute (R01EY014847, R01EY026147)
- Uehara Memorial Foundation
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Galectins and Cancer Biology
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Ocular Surface and Contact Lens
- Keywords
- galectin-3, IL-1β, keratitis, interleukin-8, interleukin-6, IL-1 receptor 1, innate immunity, epithelial inflammation
- MeSH terms
- Cells, Cultured, Endocytosis, Humans, Keratitis, Protein Binding, Keratinocytes, Galectin 3, Interleukin-1beta
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