We explored the pathological changes and the activation of local
complement system in
COVID-19 pneumonia. Lung
paraffin sections of
COVID-19 infected patients were analyzed by HE (
hematoxylin-
eosin) staining. The deposition of
complement C3, the deposition of C3b/
iC3b/C3d and
C5b-9, and the expression of
complement regulatory
proteins, CD59, CD46 and CD55 were detected by immunohistochemistry. In
COVID-19 patients' lung tissues,
fibrin exudation, mixed with erythrocyte, alveolar macrophage and shed pneumocyte are usually observed in the alveoli. The formation of an "alveolar emboli" structure may contribute to
thrombosis and consolidation in lung tissue. In addition, we also found that compared to normal tissue, the lung tissues of
COVID-19 patients displayed the hyper-activation of
complement that is represented by extensive deposition of C3, C3b/
iC3b/C3d and
C5b-9, and the increased expression level of
complement regulatory
proteins CD55, and especially CD59 but not CD46. The
thrombosis and consolidation in lung tissues may contribute to the pathogenesis of
COVID-19. The increased expression of CD55 and CD59 may reflect a feedback of self-protection on the
complement hyper-activation. Further, the increased C3 deposition and the strongly activated
complement system in lung tissues may suggest the rationale of
complement-targeted
therapeutics in conquering
COVID-19.