Targeted deletions of complement lectin pathway genes improve outcome in traumatic brain injury, with MASP-2 playing a major role.

ABSTRACT: The lectin pathway (LP) of complement activation is believed to contribute to brain inflammation. The study aims to identify the key components of the LP contributing to TBI outcome as possible novel pharmacological targets. We compared the long-term neurological deficits and neuropathology of wild-type mice (WT) to that of mice carrying gene deletions of key LP components after experimental TBI. WT or MASP-2 (Masp2^-/-), ficolin-A (Fcna^-/-), CL-11 (Colec11^-/-), MASP-1/3 (Masp1^-/-), MBL-C (Mbl2^-/-), MBL-A (Mbl1^-/-) or MBL^-/- (Mbl1^-/-/Mbl2^-/-) deficient male C57BL/6J mice were used. Mice underwent sham surgery or TBI by controlled cortical impact. The sensorimotor response was evaluated by neur

SUBMITTER: Mercurio D 

PROVIDER: S-EPMC7592565 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature