Abstract
Traumatic brain injury (TBI) is a leading cause of global morbidity and mortality, partially due to the lack of sensitive diagnostic methods and efficacious therapies. Panels of protein biomarkers have been proposed as a way of diagnosing and monitoring TBI. To measure multiple TBI biomarkers simultaneously, we present a variable height microfluidic device consisting of a single channel that varies in height between the inlet and outlet and can passively multiplex bead-based immunoassays by trapping assay beads at the point where their diameter matches the channel height. We developed bead-based quantum dot-linked immunosorbent assays (QLISAs) for interleukin-6 (IL-6), glial fibrillary acidic protein (GFAP), and interleukin-8 (IL-8) using DynabeadsTM M-450, M-270, and MyOneTM, respectively. The IL-6 and GFAP QLISAs were successfully multiplexed using a variable height channel that ranged in height from ~7.6 µm at the inlet to ~2.1 µm at the outlet. The IL-6, GFAP, and IL-8 QLISAs were also multiplexed using a channel that ranged in height from ~6.3 µm at the inlet to ~0.9 µm at the outlet. Our system can keep pace with TBI biomarker discovery and validation, as additional protein biomarkers can be multiplexed simply by adding in antibody-conjugated beads of different diameters.
Highlights
Traumatic brain injury (TBI) causes significant morbidity and mortality globally
We present bead-based quantum dot-linked immunosorbent assays (QLISAs) for glial fibrillary acidic protein (GFAP), a marker of astrocyte injury [18]; interleukin-6 (IL-6), a marker of inflammation; and interleukin-8 (IL-8), another marker of inflammation [19,20,21]
Was presented a variable height microfluidic device that is capable of passively multiplexing bead-based QLISAs for IL-6, GFAP, and IL-8, three TBI protein biomarkers
Summary
Traumatic brain injury (TBI) causes significant morbidity and mortality globally. In the United States alone, an estimated 2.87 million people sustain a TBI annually, and 50,000 of these individuals die of their injuries. 2% of the United States population is estimated to have a disability caused by TBI [1,2]. The high rates of morbidity and mortality can be attributed to inadequate diagnostic and treatment methods. Assessment of TBI injuries is typically done through neurological examination and neuroimaging techniques. While these methods may identify direct tissue damage to the brain, they are more limited in their ability to monitor secondary damage stemming from the initial injury. The primary tissue damage sets off a cascade of secondary injuries, such as neuronal cell death, blood–brain barrier breakdown, edema, and upregulation of inflammatory markers [4,5]
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