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Updated: Apr 30, 2026
Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
Published on: September 4, 2013
Mannose-binding lectin is expressed after clinical and experimental traumatic brain injury and its deletion is
Luca Longhi1, Franca Orsini, Daiana De Blasio
11Department of Pathophysiology and Transplantation, Neurosurgical Intensive Care Unit, University of Milano, Fondazione IRCCS Ca' Granda-Ospedale Maggiore Policlinico, Milano, Italy. 2Department of Neuroscience, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Milano, Italy. 3Department of Biomedical Sciences, University of Chieti, Pescara, Italy. 4Department of Neurosurgery, Fondazione IRCCS Ca'Granda-Ospedale Maggiore Policlinico, Milano, Italy.
Objective:
Mannose-binding lectin protein is the activator of the lectin complement pathway. Goals were (1) to investigate mannose-binding lectin expression after human and experimental traumatic brain injury induced by controlled cortical impact and (2) to evaluate whether mannose-binding lectin deletion is associated with reduced sequelae after controlled cortical impact.
Design:
Translational research, combining a human/experimental observational study and a prospective experimental study.
Setting:
University hospital/research laboratory.
Patients And Subjects:
Brain-injured patients, C57Bl/6 mice, and mannose-binding lectin-A and mannose-binding lectin-C double-knockout (-/-) mice.
Interventions:
Using anti-human mannose-binding lectin antibody, we evaluated mannose-binding lectin expression in tissue samples from six patients who underwent surgery for a cerebral contusion. Immunohistochemistry was also performed on tissues obtained from mice at 30 minutes; 6, 12, 24, 48, and 96 hours; and 1 week after controlled cortical impact using anti-mouse mannose-binding lectin-A and mannose-binding lectin-C antibodies. We evaluated the effects of mannose-binding lectin deletion in wild-type and mannose-binding lectin-A and mannose-binding lectin-C double-knockout mice. Functional outcome was evaluated using the neuroscore and beam walk tests for 4 weeks postinjury (n = 11). Histological injury was evaluated by comparing neuronal cell counts in the cortex adjacent to the contusion (n = 11).
Measurements And Main Results:
Following human traumatic brain injury, we observed mannose-binding lectin-positive immunostaining in the injured cortex as early as few hours and up to 5 days postinjury. Similarly in mice, we observed mannose-binding lectin-C-positive immunoreactivity in the injured cortex beginning 30 minutes and persisting up to 1 week postinjury. The extent of mannose-binding lectin-A expression was lower when compared with that of mannose-binding lectin-C. We observed attenuated sensorimotor deficits in mannose-binding lectin (-/-) mice compared with wild-type mice at 2-4 weeks postinjury. Furthermore, we observed reduced cortical cell loss at 5 weeks postinjury in mannose-binding lectin (-/-) mice compared with wild-type mice.
Conclusions:
Mannose-binding lectin expression was documented after traumatic brain injury. The reduced sequelae associated with mannose-binding lectin absence suggest that mannose-binding lectin modulation might be a potential target after traumatic brain injury.
