Activation of the human contact pathway by bacterial cell envelope components. Bacterial lysis releases membrane components such as LPS, PGN, and LTA, which interact with FXII and promote its activation to FXIIa. FXIIa initiates the intrinsic coagulation pathway by generating FXIa, contributing to thrombosis. FXIIa also activates plasma kallikrein (PKa), triggering the kallikrein-kinin system and leading to the release of the proinflammatory peptide bradykinin. In addition, FXIIa, FXIa, and PKa have a suggestive of a role in the host defense mechanism.