Abstract Complement inhibition is exploited by extracellular pathogens to combat clearance. Borreliella burgdorferi, the causative agent of Lyme disease, harnesses complement evasion techniques to establish and maintain infection in mammalian hosts. B. burgdorferi encodes bbk32, a surface lipoprotein that binds extracellular matrix (ECM) components, specifically glycosoaminoglycans (GAGs) and fibronectin (Fn) within its amino terminus.