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Normal but not altered mucins activate neutrophils.
Marie-Laure Rachel Aknin1, Monica Berry, Andrew David Dick
1Department of Clinical Sciences, Ophthalmology, Bristol Eye Hospital, University of Bristol, BS1 2LX, Bristol, UK. ml.aknin@bristol.ac.uk
Cell and Tissue Research
|October 19, 2004
Summary
Changes in ocular mucins, common in dry eye disease, alter neutrophil activation. Normal mucins promote neutrophil oxidative burst, while dry eye mucins do not, suggesting immune interplay at the ocular surface.
Area of Science:
- Ocular immunology
- Cellular immunology
- Glycobiology
Background:
- Leukocyte interactions with their environment are mediated by oligosaccharide epitopes found on ocular mucins.
- Neutrophils are the primary immune cells in the inflamed ocular surface environment during sleep.
- Dry eye disease is associated with changes in mucin glycosylation.
Purpose of the Study:
- To investigate how alterations in mucin glycosylation, as seen in dry eye, affect neutrophil phenotype and activation.
- To explore the reciprocal influences between the ocular surface environment and systemic immunity.
Main Methods:
- Peripheral blood leukocytes were flowed over ocular surface mucins from normal and dry eye patients.
- Cells were analyzed using flow cytometry with fluorescent antibodies.
- Oxidative burst was assessed using dihydrorhodamine.
Main Results:
- Normal mucins decreased neutrophil cathepsin G fluorescence at physiological flow rates, an effect not seen with dry eye mucins.
- Normal mucins induced an oxidative burst in neutrophils.
- Dry eye mucins showed fluorescence in adherent intact cells, indicating altered neutrophil interaction.
Conclusions:
- Differences in neutrophil activation by normal versus pathological mucins highlight immune system interplay.
- Ocular mucin glycosylation plays a role in modulating neutrophil responses.
- These findings suggest a link between local ocular immunity and systemic immune regulation.