Research Reports - Bone fracture enhances trauma brain injury

Scand J Immunol. 2015 Oct 8. doi: 10.1111/sji.12393. [Epub ahead of print]

Yang L(1), Guo Y(2), Wen D(3), Yang L(4), Chen Y(1), Zhang G(1), Fan Z(1).

Traumatic brain injury (TBI) is one of the leading causes of mortality and
morbidity in young individuals worldwide. However, the understanding of TBI at
secondary phase remained obscure and more knowledge of the pathophysiology of TBI
is necessary. In present study, we examined the influence of bone fracture (BF)
on TBI and investigated whether blocking high mobility group 1 (HMGB1) protein,
an inflammatory mediator, could be effective to alleviate TBI. We found
neurological severity was significantly increased by BF at 4 days post TBI with
longer removal time of adhesive tape and higher percentage of left turn in the
corner test compared to TBI treatment alone. Additionally, higher brain lesion
volume and severer brain edema in TBI + BF mice supports the negative effect of
BF on TBI. HMGB1 level was significantly stimulated by BF, suggesting the
important role of HMGB1 in the development of secondary TBI. Notably, ablation of
HMGB1 significantly reduced this negative influence of BF on TBI. These results
suggest that HMGB1 can be massively induced by the systemic immune activation
triggered by BF, which in turn aggravates inflammation. Blocking HMGB1 reduced
the inflammatory effect of BF and therefore helps lessen the severity of
secondary TBI. In conclusion, these results provided the evidence that anti-HMGB1
may be an effective and feasible method to alleviate TBI. This article is
protected by copyright. All rights reserved.

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