In contrast, almost 60% of the mice not yet displaying high C3 or auto-antibody levels were rescued by complement depletion (Supporting Information Fig S4A and B and Fig 7C), showing significantly reduced auto-antibody titres, heart infiltration and fibrosis (Supporting Information Fig S4C E).
And in rats, complement depletion during passive transfer at the lung stage significantly reduced protection, thus generation of C3a and C5a by antibody/antigen fixation of complement may play a role [7].
Therefore, experiments were designed to test the effect of complement depletion on cerebral infarct volume in adult rats and cerebral atrophy in neonatal rats.
Complement depletion by treatment with cobra venom [ 109] and prevention of complement activation with nafamostat mesilate, a serine protease inhibitor, reduced vasospasm in experimental models [ 90, 110] and human subjects [ 111, 112].
Although the pathology of AAV contains few immune deposits, complement depletion has abrogated experimental myeloperoxidase-ANCA renal vasculitis and is a potential target in human disease.
Complement depletion induced by CVF significantly reduced post-ischemic cerebral infarct volume and atrophy in adult and neonatal rats.
Moreover, complement depletion or inhibition demonstrated beneficial effects in animal models of hemorrhage, and therefore they represent an interesting novel treatment option [ 162] in the clinical arena.
In case of complement depletion, the survival of donor myoblasts was not enhanced so that it was argued that complement could induce the activity of neutrophils and macrophages, indirectly regulating the death of transplanted cells [ 115].
A study by Hällstrom et al. showed a correlation between complement resistance and disease severity but no difference in complement resistance between invasive and colonizing NTHi strains (30 ).
Studies in complement-deficient individuals have indicated a strong association between complement deficiencies and infections or with immune complex disease and autoimmunity.
