TY - JOUR
T1 - Mincle signaling in the innate immune response after traumatic brain injury
AU - de Rivero Vaccari, Juan Pablo P
AU - De Rivero Vaccari, Juan Carlos
AU - Brand, Frank J.
AU - Berti, Aldo F.
AU - Alonso, Ofelia F.
AU - Bullock, Ross
PY - 2015/2/15
Y1 - 2015/2/15
N2 - The innate immune response contributes to the inflammatory activity after traumatic brain injury (TBI). In the present study we identify macrophage-inducible C-type lectin (mincle) as a pattern recognition receptor that contributes to innate immunity in neurons after TBI. Here we report that mincle is activated by SAP130 in cortical neurons in culture, resulting in production of the inflammatory cytokine TNF. In addition, mincle and SAP130 are elevated in the brain and cerebrospinal fluid of humans after TBI and the brain of rodents after fluid percussion brain injury. Thus, these findings suggest the involvement of mincle to the pathology of TBI. Importantly, blocking mincle with a neutralizing antibody against mincle in cortical neurons in culture treated with SAP130 resulted in inhibition of mincle signaling and decreased TNF production. Therefore, our findings identify mincle as a contributor to the inflammatory response after TBI.
AB - The innate immune response contributes to the inflammatory activity after traumatic brain injury (TBI). In the present study we identify macrophage-inducible C-type lectin (mincle) as a pattern recognition receptor that contributes to innate immunity in neurons after TBI. Here we report that mincle is activated by SAP130 in cortical neurons in culture, resulting in production of the inflammatory cytokine TNF. In addition, mincle and SAP130 are elevated in the brain and cerebrospinal fluid of humans after TBI and the brain of rodents after fluid percussion brain injury. Thus, these findings suggest the involvement of mincle to the pathology of TBI. Importantly, blocking mincle with a neutralizing antibody against mincle in cortical neurons in culture treated with SAP130 resulted in inhibition of mincle signaling and decreased TNF production. Therefore, our findings identify mincle as a contributor to the inflammatory response after TBI.
KW - innate immunity
KW - mincle
KW - neuroinflammation
KW - neurons
KW - traumatic brain injury
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U2 - 10.1089/neu.2014.3436
DO - 10.1089/neu.2014.3436
M3 - Article
C2 - 25111533
AN - SCOPUS:84923274977
VL - 32
SP - 228
EP - 236
JO - Journal of Neurotrauma
JF - Journal of Neurotrauma
SN - 0897-7151
IS - 4
ER -