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Complement and polymorphonuclear leukocytes do not determine the vascular permeability induced by intraocular LPS.
The American Journal of Pathology
|January 1, 1985
Summary
Ocular inflammation induced by Escherichia coli endotoxin (LPS) in rabbits is not dependent on polymorphonuclear leukocytes (PMNs) or complement. Aqueous humor contains PMN-attracting activity not primarily mediated by C5a.
Area of Science:
- Ophthalmology
- Immunology
- Inflammation Research
Background:
- Intravitreal injection of Escherichia coli endotoxin (LPS) induces ocular inflammation in rabbits.
- This inflammation involves increased ocular vascular permeability (OVP) and leukocyte infiltration, primarily polymorphonuclear leukocytes (PMNs).
Purpose of the Study:
- To investigate the roles of PMNs and complement in LPS-induced ocular inflammation and OVP.
- To characterize the chemotactic activity present in the aqueous humor during ocular inflammation.
Main Methods:
- Rabbits were treated with nitrogen mustard to deplete PMNs or with cobra venom factor (CVF) to deplete complement prior to LPS injection.
- Ocular vascular permeability was measured by 125I-albumin extravasation.
- Histopathology was used to assess leukocyte infiltration.
- Complement activity and chemotactic activity in serum and aqueous humor were measured.
Main Results:
- PMN depletion did not alter LPS-induced OVP.
- Complement depletion (using CVF) did not affect LPS-induced OVP, although it did affect a passive Arthus reaction.
- Chemotactic activity for rabbit PMNs was present in the aqueous humor of both control and CVF-treated rabbits and was not primarily C5a-mediated.
Conclusions:
- Neither circulating PMNs nor complement are the primary determinants of ocular vascular permeability following intravitreous LPS injection.
- The chemotactic activity in the aqueous humor during ocular inflammation is not mainly C5a and attracts rabbit PMNs.