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Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Professor Anat Galor, University of Miami,
- Second opponent: Professor Jesmond Dalli, Queen Mary University of London,
- Third member and chair of the evaluation committee: Professor Knut Tomas Dalen, University of Oslo
Chair of the Defence
Professor emeritus Trond Buanes, University of Oslo
Principal Supervisor
Professor II Tor Paaske Utheim, Universitetet i Oslo
Summary
This thesis explores ocular surface biology and the science of how inflammation is actively brought to an end (“resolution”).
We asked whether two of the body’s own pro-resolving mediators—Annexin A1 and Maresin-1—can help the eye end inflammation and stabilize the tear film. The focus was the conjunctival goblet cell, a mucin-producing cell that keeps the surface smooth and protected. We tested whether these mediators raise intracellular calcium (the on-switch for secretion), increase release of the main tear mucus, and tone down histamine-driven over-secretion seen in allergy.
We studied primary goblet cells from rat conjunctiva, measuring single-cell calcium and mucin release, and used receptor and pathway blockers to probe mechanisms. Annexin A1 increased calcium and mucin release; short Annexin-derived peptides partly reproduced these effects and reduced histamine signaling. Maresin-1 likewise increased calcium and mucin. Pre-exposure to either mediator made cells less responsive to histamine.
Overall, these signals act as “two-way” regulators: they support normal mucin production in health and actively rein in allergy-driven excess, suggesting a route to stabilize the tear film in allergic conjunctivitis (less mucin) and dry eye disease (more mucin).
Additional information
Contact the research support staff.