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Published on: October 20, 2023
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Sialylation regulates neutrophil transepithelial migration, CD11b/CD18 activation, and intestinal mucosal
Veronica Azcutia1, Matthias Kelm1, Dylan Fink1
1Department of Pathology, University of Michigan, Ann Arbor, Michigan, USA.
JCI Insight
|January 31, 2023
Summary
Sialic acid on CD11b/CD18 regulates polymorphonuclear neutrophil (PMN) migration and inflammatory functions. Inhibiting sialic acid removal reduces PMN influx and tissue damage, offering new therapeutic targets for inflammatory diseases.
Area of Science:
- Immunology
- Cell Biology
- Glycobiology
Background:
- Polymorphonuclear neutrophils (PMNs) are crucial for host defense but their dysregulated migration causes inflammatory mucosal diseases.
- Transepithelial migration (TEpM) is the final step of PMN influx into mucosal organs.
- While fucose and GlcNAc glycans on CD11b/CD18 are known regulators, the role of sialic acid (Sia) is unclear.
Purpose of the Study:
- To investigate the role of sialic acid (Sia) on CD11b/CD18 in regulating PMN transepithelial migration (TEpM).
- To determine how sialylation affects PMN inflammatory functions.
- To explore the potential of targeting sialic acid for treating inflammatory mucosal diseases.
Main Methods:
- In vitro and in vivo models of PMN migration across intestinal epithelium.
- Analysis of PMN degranulation and superoxide release.
- Assessment of CD11b/CD18 activation and downstream signaling pathways (Syk, p38 MAPK).
Main Results:
- Inhibiting sialidase-mediated removal of α2-3-linked Sia from CD11b/CD18 blocked PMN TEpM.
- Sialylation modulated PMN degranulation and superoxide release.
- Sialidase inhibition reduced bacterial peptide-induced CD11b/CD18 activation and downstream signaling.
Conclusions:
- Sialic acid on CD11b/CD18 is a key regulator of PMN migration and inflammatory functions.
- Targeting sialic acid or sialidases may offer novel therapeutic strategies for inflammatory mucosal diseases.
- Sialylated glycans on CD11b/CD18 are potential targets to reduce PMN-mediated tissue damage.
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