The role of coagulation-fibrinolysis system in
experimental autoimmune encephalomyelitis (EAE) was studied by using
batroxobin, derived from the
venom of the South American pit viper Bothrops atrox moojeni.
Batroxobin converts circulating
fibrinogen into an insoluble form and causes a profound degree of
afibrinogenemia.
Batroxobin treatment (30 BU/kg/day) suppressed clinical signs of cell transferred EAE; the mean cumulative clinical score for
batroxobin treated rats was 3.97, while saline treated controls scored 6.9 (P < 0.01). Plasma
fibrinogen concentration decreased significantly in
batroxobin-treated rats. Histologically, the degree of perivascular mononuclear cell infiltration in the spinal cord was not suppressed in
batroxobin-treated rats compared to saline-treated control rats, however, deposition of
fibrin around the vessels in the spinal cord was markedly suppressed in
batroxobin-treated rats. These findings suggest that
batroxobin suppresses EAE by preventing
fibrin deposition, and provide evidence that CNS-associated deposition of
fibrin and ensuing fibrinolysis, together with increased permeability of blood brain barrier (BBB), are related prerequisites for the clinical manifestation of EAE.