Experimental Endophthalmitis Phacoanaphylactica in Rabbits

Burky, Earl L.

doi:10.1001/archopht.1934.00830170074009

Cited by 45 publications

(7 citation statements)

References 4 publications

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“…This is in keeping with the concept that heterologous antibodies are less pathogenetic than autoantibodies and that previous attempts to produce such inflammation resulted in variable and often unpredictable changes, and never typical granulomatous inflammation around the lens (Verhoeff and Lemoine, 1922;Burky, 1934;Scobee and Slaughter, 1944;Muller, 1952). It is known that the insoluble albuminoid is more potent than soluble lens crystallins in inducing T-cell sensitisation and therefore delayed tissue allergy (Manski, 1973).…”

supporting

confidence: 79%

Immunopathology of the lens. I. Humoral and cellular immune responses to heterologous lens antigens and their roles in ocular inflammation.

Rahi¹,

Misra²,

Morgan³

1977

British Journal of Ophthalmology

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SUMMARY In experimental rabbits heterologous soluble lens proteins consisting of a-, 3-, and y-crystallins were found to be antigenic; they stimulated a marked antibody response compared to a rather weak T-cell response. The serum antibodies to ac-crystallins appeared first, to be followed by antibodies to 13-and y-crystallins in that order. The rabbits did not respond to heterologous y-crystallins unless these were injected with Freund's adjuvant containing mycobacteria. Incomplete Freund's adjuvant (i.e., without mycobacteria) was found to be an inferior immunoaccelerator so far as lens antigens are concerned. The response to lenticular antigens in both magnitude and duration varied in different rabbits, which suggested to us the important role played by a central control mechanism involving the immune response (Ir) genes.Some of the antibodies in potent lens antisera cross-reacted with mitochondria, endoplasmic reticulum (i.e., microsomes), contractile organelles, and cell nuclei. This explains for the first time at least in part the reasons for the widely observed phenomenon of the reactivity of lens antisera with ocular and extraocular structures. Antibodies to soluble lens proteins as detected by immunofluorescence and immunoperoxidase techniques were shown to be of the IgG class. Systemic heterologous immunisation followed by discission of the lens does not lead to the typical changes of phakoallergic endophthalmitis in the rabbit.

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supporting

confidence: 79%

Immunopathology of the lens. I. Humoral and cellular immune responses to heterologous lens antigens and their roles in ocular inflammation.

Rahi¹,

Misra²,

Morgan³

1977

British Journal of Ophthalmology

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“…Lens‐induced uveitis (LIU) has been described as a naturally occurring disease in many animal species including dogs, cats, rabbits, rats, birds, horses and a calf 1 –18 . It has been experimentally produced in laboratory animals 19 –25 . It was first reported in human beings over 75 years ago 26…”

Section: Introductionmentioning

confidence: 99%

Lens‐induced uveitis

Woerdt

2000

Veterinary Ophthalmology

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has been described in humans and many animal species. Traumatic rupture of the lens capsule may result in vision-threatening intraocular inflammation that is poorly responsive to medical management. Phthisis bulbi, persistent uveitis or glaucoma often occurs in these eyes. Surgical removal of the lens material is generally indicated shortly after the injury in an effort to preserve vision. Leaking of lens proteins through an intact lens capsule may result in a lympho-plasmacytic anterior uveitis. This is most commonly associated with the presence of a hypermature cataract. The presence of lens-induced uveitis prior to cataract surgery significantly reduces the success rate of cataract surgery. Small amounts of circulating lens proteins maintain a normal T-cell tolerance for lens proteins. Lens-induced uveitis develops when a breakdown occurs of this normal T-cell tolerance. Immune complexes play an important role in the tissue damage associated with the ensuing inflammation. Other factors associated with the tissue damage include hydroxyl radicals, nitroxide radicals, and hydrogen peroxide and arachidonic acid metabolites. Treatment consists of topical and systemic anti-inflammatory medications, mydriatic agents, and glaucoma medications when indicated. Experimental pharmacological agents include dual cyclooxygenase/lipoxygenase inhibitors, interleukin-1 blockers, antioxidants and hydroxyl radical scavengers.

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“…The resulting inflammatory reaction is thought to be an autoimmune response to those proteins. In the animal models, the lens is punctured artificially after the immunization with the lens protein [154,155]. Clinically, experimental lens-induced uveitis is characterized by anterior chamber inflammation and flare.…”

Section: Lens-induced Uveitismentioning

confidence: 99%