Gene expression profiling in stroke: relevance of blood-brain interaction

Abstract

Biomarker profiling is utilized to identify diagnostic and prognostic candidates for stroke. Clinical and preclinical biomarker data suggest altered circulating immune responses may illuminate the mechanisms of stroke recovery. However, the relationship between peripheral blood biomarker profile(s) and brain profiles following stroke remains elusive. Data show that neutrophil lymphocyte ratio (NLR) predicts stroke outcome. Neutrophils release Arginase 1 (ARG1) resulting in T lymphocyte suppression in peripheral blood. Interestingly, the cellular response to stroke may have implications for known biomarker profiles. Conversely, preclinical evidence suggests that upregulation of ARG1 in microglia is a marker of M2 macrophages and may influence neuroprotection. Comparing clinical and preclinical studies creates opportunities to explore the molecular mechanisms of blood and brain biomarker interactions in stroke.

Figure 1

Stroke not only induces alterations of peripheral blood profiling, but also produces changes in the immune system. A) Blood samples can be collected from stroke patients to obtain peripheral blood profiles. Dynamic inflammatory response requires multiple time course sampling to identify subcategories of stroke events, to predict patients' outcome and to develop new biomarkers in stratification and diagnosis of stroke. Samples from multiple organs can be collected from preclinical stroke models to describe stroke phenotype, obtain the gene expression changes and their associated with brain damage. B) Stroke induces rapid activation of the peripheral immune system and subsequent immunosuppressive phase.