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WAM Essentials, Inc.
Systemic Enzyme Therapy
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Enzyme therapy of experimental glomerulonephritis
Emancipator S.N. and Lamm M.E.
Institute of Pathology, Case Western Reserve University
Cleveland, Ohio 44106, U.S.A.
In: Current Therapy in Nephrology, 1989, pp 582 - Vydavatel:
Kluwer Academic publishers - (Cleveland)
80 KA |
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Glomerulonephritis (GN), resulting from the
deposition or formation of immune complexes (IC) within glomeruli,
is often progressive and represents a major public health
problem worldwide (1). Although progress within the last
decade has helped to elucidate the pathogenesis of GN, therapy
remains limited. Several mechanisms and inflammatory mediators
are capable of contributing to disease, apparently operative
in different combinations in the various patterns of GN (2).
Therapy directed at particular pathways is consequently restricted
in scope and may be of limited potential.
We reasoned that digestion of glomerular immune deposits
by enzymes could, to the extent that such deposits elicit
GN, ameliorate the signs of disease and perhaps retard progression.
Our earlier studies showed that non-toxic doses of proteolytic
enzymes could markedly decrease IC deposits in the glomerular
capillaries or mesangium in passive serum sickness GN models
induced by injection of preformed IC of bovine gamma globulin
(BGG) and rabbit antibody to BGG (3). Mice or rats treated
systemically with mixtures of chymopapain and subtilisin
did not display the intense immunofluorescence deposits seen
in animals given the same amounts of IC but treated with
saline instead of enzymes. The distribution of fluorescence
intensities of rabbit antibodies in treated animals was significantly
shifted to negative or low-grade scores compared to saline
treated subjects, and antigen deposits were also significantly
attenuated. We also quantified glomerular IC in rats given
complexes of BGG antigen and radioactive rabbit anti-BGG
and found that glomeruli from enzyme-treated rats contained
only half the radioactivity present in rats treated with
saline.
In the active serum sickness model, rats given targeted
or untargeted enzyme therapy for 5 days had significantly
less proteinuria than saline-treated controls, despite the
fact that protein excretion prior to treatment (84.6 ± 11.9
mg/day) was not different among the groups (F = 1.3). Rats
given the naturally cationic avidin, which binds electrostatically
to glomerular capillaries, and then given biotinyl protease
capable of binding tightly to the avidin, had significantly
less proteinuria than rats given nontargeted proteases, either
biotinyl protease alone or unmodified protease plus avidin.
Moreover, rats given protease targeted to glomerular capillaries
by avidin and biotin had the least intense glomerular deposits
by immunofluorescence of all the groups (data not shown).
The benefits of protease therapy are additionally evident
in their amelioration of the hypercholesterolemia associated
with the nephrotic syndrome in these rats (normal rat serum
cholesterol is 98 ± 4.2 mg/dl). Again, targeted protease
was significantly better than nontargeted protease. |
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