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  • Poster presentation
  • Open Access

Mannose binding lectin deficiency attenuates neurobehavioral deficits following experimental traumatic brain injury

  • 1,
  • 2,
  • 2,
  • 1 and
  • 2
Critical Care201216 (Suppl 1) :P300

  • Published:


  • Traumatic Brain Injury
  • Mannose Binding Lectin
  • Control Cortical Impact
  • Secondary Brain Damage
  • Experimental Traumatic Brain Injury


Mannose binding lectin (MBL) is the activator of the lectin complement pathway. After cerebral ischemia it has been shown that MBL could be a mediator of secondary brain damage, in contrast after traumatic brain injury (TBI) there are data suggesting that it could be linked to neuroprotection. We tested the hypothesis that MBL is involved in the pathophysiology of TBI. We characterized (1) the temporal activation of MBL and (2) the effects of its inhibition in a model of experimental TBI.


(1) Male C57/Bl6 mice were subjected to intraperitoneal anesthesia (pentobarbital, 65 mg/kg) followed by the controlled cortical impact brain injury model of experimental TBI (injury parameters: velocity of 5 m/second and 1 mm depth of deformation). MBL immunostaining was evaluated at various time points after TBI: 30 minutes, 1, 6, 12, 24, 48, 96 hours and 1 week using anti MBL-A and MBL-C antibodies (n = 3). (2) The effects of MBL inhibition were evaluated by comparing functional and histologic outcomes in C57/Bl6 mice (WT) and in MBL knockout (-/-) mice. Functional outcome was tested using the Composite Neuroscore and Beam Walk test weekly up to 4 weeks postinjury (n = 11). Histologic outcome was evaluated by calculating the contusion volume at 4 weeks postinjury (n = 6). Sham-operated mice received identical anesthesia without brain injury.


We observed a robust MBL-positive immunostaining in the injured cerebral cortex starting at 30 minutes postinjury and up to 1 week, suggestive of an activation of this pathway following TBI. MBL was observed both at endothelial and tissue levels. Consistently, injured WT and MBL (-/-) mice showed neurological motor deficits up to 4 weeks postinjury when compared to their sham controls. Notably, MBL (-/-) mice showed attenuated behavioral deficits when compared to their WT counterpart at 2 to 4 weeks postinjury (P < 0.01 for both Neuroscore and Beam Walk test). In contrast we observed similar contusion volumes at 4 weeks postinjury (WT = 15.6 ± 3.2 cm3 and MBL KO = 13.9 ± 3.2 cm3, P = 0.3).


We observed that: (1) MBL deposition and/or synthesis is increased following TBI; and (2) MBL deficiency is associated with functional neuroprotection, suggesting that MBL modulation might be a potential therapeutic target after TBI.

Authors’ Affiliations

University of Milano, Milan, Italy
Mario Negri Institute, Milan, Italy


© Longhi et al.; licensee BioMed Central Ltd. 2012

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.