Ocular Surface Inflammation
Ocular Surface Inflammation - Related Videos
03:06
A Method to Induce Ocular Surface Inflammation in a Murine Model
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2025
This video demonstrates a method to induce ocular surface inflammation and meibomian gland dysfunction in a murine model. Stimulation of the mouse's immune system using an immunogen and later restimulation with the same immunogen promotes ocular surface inflammation, which causes plugging of meibomian gland secretion through neutrophil-produced aggNETs and leads to dry eye disease.
06:38
Induction of Ocular Surface Inflammation and Collection of Involved Tissues
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Cited by 2 •
2022
Ocular surface inflammation harms the ocular surface tissues and compromises vital functions of the eye. The present protocol describes a method to induce ocular inflammation and collect compromised tissues in a mouse model of Meibomian gland dysfunction (MGD).
01:38
Inflammation
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2019
Overview In response to tissue injury and infection, mast cells initiate inflammation. Mast cells release chemicals that increase the permeability of adjacent blood capillaries and attract additional immune cells to the wound or site of infection. Neutrophils are phagocytic leukocytes that exit the bloodstream and engulf invading microbes. Blood clotting platelets seal the wound and fibers create a scaffold for wound healing. Macrophages engulf aging neutrophils to end the acute inflammatory...
03:40
Nasolacrimal Lavage as a Treatment for Ocular Surface Toxic Soup Syndrome
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Cited by 1 •
2025
OSTSS leads to pooled inflammatory mediators in the tear film, causing symptoms like epiphora and discomfort. Here, we present a case where therapeutic nasolacrimal lavage every 2 months resolved epiphora and itchiness, suggesting its efficacy as a therapeutic intervention for OSTSS. Additionally, we report subjective improvements in symptoms in 3 additional patients.
06:35
Experimental Glaucoma Induced by Ocular Injection of Magnetic Microspheres
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Cited by 25 •
2015
We present a method for inducing elevated intraocular pressure (IOP), by injecting magnetic microspheres into the rat eye, to model glaucoma. This leads to strong pressure rises, and extensive neuronal death. This protocol is easy to perform, does not require repeat injections, and produces stable long-lasting IOP rises.
FAQs
Epithelial and immune cells release cytokines and chemokines after detecting microbial components or tissue damage. These mediators recruit leukocytes to the ocular surface, coordinating host defense but also influencing the tear film and corneal barrier. Studying their release helps researchers connect an initiating stimulus with cellular recruitment and the resulting balance between protection and tissue disruption.
Regulatory pathways limit the intensity and duration of the immune response at the ocular surface. Without adequate control, leukocyte recruitment and inflammatory signaling can contribute to tear-film alteration and corneal barrier disruption. Their protective role is therefore central to distinguishing a useful defense against harmful stimuli from inflammation that threatens the tissues needed for clear vision.
The same inflammatory response may be associated with infection, allergy, injury, or chronic surface disease, so inflammatory findings must be interpreted in context. Research compares responses to microbial components with responses to tissue damage and other surface stresses. This distinction helps clarify whether inflammation primarily reflects host defense, a noninfectious trigger, or persistent surface pathology.
Pathogens, the resident microbiota, and environmental stress can each influence interactions between the ocular surface and the immune system. Their contributions are studied to determine how surface conditions alter inflammatory signaling and barrier integrity. This broader context is important because ocular inflammation may arise from combined microbial and environmental influences rather than from a single isolated cause.
Researchers examine interactions among microbial components, tissue damage, epithelial cells, immune cells, leukocytes, and the tear-film tissues. They use these relationships to distinguish protective host defense from damaging inflammation and to assess effects on the corneal barrier. This investigative framework connects initiating signals with tissue outcomes and supports interpretation across infectious and noninfectious surface conditions.
Characterizing ocular surface immune interactions can support biomarker development and more targeted anti-inflammatory or antimicrobial treatments. Biomarkers may help describe inflammatory activity or distinguish relevant processes, while targeted therapies aim to address damaging inflammation or microbial contributors. The overall goal is to preserve protective defense while reducing effects that disrupt the tear film or corneal barrier.