Role of Pneumococcal NanA Neuraminidase Activity in Peripheral Blood.

The most frequent form of hemolytic-uremic syndrome (HUS) is associated with infections caused by Shiga-like toxin-producing Enterohaemorrhagic (STEC). In rarer cases HUS can be triggered by . While production of Shiga-like toxins explains STEC-HUS, the mechanisms of pneumococcal HUS are less well-known produces neuraminidases with activity against cell surface sialic acids that are critical for factor H-mediated complement regulation on cells and platelets.

Complement Factor H and Apolipoprotein E Participate in Regulation of Inflammation in THP-1 Macrophages.

The alternative pathway (AP) of complement is constantly active in plasma and can easily be activated on self surfaces and trigger local inflammation. Host cells are protected from AP attack by Factor H (FH), the main AP regulator in plasma. Although complement is known to play a role in atherosclerosis, the mechanisms of its contribution are not fully understood.