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Significance Transendothelial trafficking of immune cells into the central nervous system (CNS) is a pathophysiological hallmark of neuroinflammatory disorders like multiple sclerosis (MS). Recent evidence suggests that the coagulation and kallikrein-kinin cascade might participate in this process. Here, we identify plasma kallikrein (KK) as a direct modulator of blood–brain barrier function in a protease-activated receptor-2–dependent manner, amplifying leukocyte trafficking into the CNS. Consequently, a deficiency of plasma prekallikrein (PK), the precursor of KK, renders mice less susceptible to experimental autoimmune encephalomyelitis (model of MS). Furthermore, PK levels were markedly enhanced in CNS lesions of MS patients. In summary, our study indicates that KK inhibition can decrease cell invasion during neuroinflammation and may offer a strategy to combat MS.

Plasma kallikrein modulates immune cell trafficking during neuroinflammation via PAR2 and bradykinin release