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Fig. 3 | Critical Care

Fig. 3

From: Fluid proteomics of CSF and serum reveal important neuroinflammatory proteins in blood–brain barrier disruption and outcome prediction following severe traumatic brain injury: a prospective, observational study

Fig. 3

BBB disruption co-occurs with upregulation of innate immune pathways, notably the complement cascade. A severe TBI elicited an acute BBB disruption among a subset of patients, quantified using QA (a). Among the n = 114 proteins significantly correlated with QA, the majority were nervous system or immune system enriched (b). Using hierarchical clustering on CSF and serum protein measurements respectively, protein levels clearly clustered depending on BBB integrity status in CSF (c), but less so in serum (d). APOE carrier status was not associated with protein levels in either group (c, d). In CSF, this corresponded to pathway upregulation of predominantly innate immune mechanisms (e). Examining proteomic profiles between patients with disrupted and intact BBB, a handful of proteins were significant in CSF (f) and merely one in serum (g). APOE Apolipoprotein E, CSF cerebrospinal fluid, CNS central nervous system, GOS Glasgow Outcome Score, MFI median fluorescence intensity, QA albumin quotient, TBI traumatic brain injury. All full protein names are given in Additional file 3: Table S1

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