Relating to an episode of corneal abrasion, leading to diagnosis at an eye hospital in London, requiring steroids to recover from daily symptoms, however reactivity of the eye to irritants has never recovers. This raises questions as to the clustering and persistence of immune cells at the site of injury. A previous post was written describing the steroid treatment and subsequent gastritis-type issues seemingly caused by the treatment.
- Do immune cells cluster at a higher density at the site of corneal abrasions?
- If so, at what rate do immune cells appear and disappear from the site of injury, and what factors influence this?
- Do steroids reduce the density of immune cells, suppress inflammatory mediator release, or both?
- Is early use of steroid more likely to affect clustering behaviour, or does it have no effect?
- Is persistent immune reactivity near the site of injury recorded in other patients?
- If so, is it considered a likely outcome for corneal abrasion?
- If not, is it more likely that individuals with immune-related disorders present with long-term reactivity?
Curtis Holt - Studio / Lab 