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Bacterial complement evasion strategies

As a first line of defense against pathogens and a mediator between innate and adaptive immunity, complement is a particular focus of evasion strategies developed by pathogens. 

We showed that one common strategy is to bind complement inhibitor C4BP, which leads to decreased opsonisation of bacteria with C3b impairing phagocytosis and allowing bacterial survival. It appears that binding of C4BP is a general mechanism of protection used by bacteria that come into contact with blood or mucosal secretions. Resistance to killing by serum and binding of C4BP is observed mostly in virulent strains that cause disseminated infections. 

Another important mechanism by which bacteria resist human complement is the production of proteases that efficiently degrade complement components. We showed this for Porphyromonas gingivalisPrevotella intermedia and very rarely studied due to great difficulties of culturing Tanerella forsythia, which all cause periodontitis and are exceptionally resistant to complement. We also identified a unique mechanism to battle complement used by the respiratory pathogen Moraxella catarrhalis. These bacteria use the surface protein Usp2 to capture and incapacitate the major complement factor C3.

Our current specific goals for this project are to understand:

the mechanisms by which bacteria circumvent attack from the complement system such as production of own complement inhibitors targeting various stages of the complement cascade or capturing host complement inhibitors

how do human complement inhibitors, commonly captured by bacterial pathogens, regulate immune responses such as inflammasome activation and monocyte differentiation

how does intracellular complement contribute to (xeno)autophagy