Role of Basigin as an Immune Mediator in the CNS

The Role of Basigin as an Immune Mediator in the CNS poster



Research Authorship:

Alicia Gonzalez and Judith D. Ochrietor

Faculty Mentor:

Dr. Judith D. Ochrietor | College of Arts and Sciences | Department of Biology


Chronic inflammation is a hallmark of many neurodegenerative disorders. Although the central nervous system (CNS) can stave peripheral pathogens from crossing the blood-brain barrier (BBB) through a network of endothelia, astrocytes, and pericytes, prolonged exposure to a pathogen can comprise this barrier, leading to an infiltration of cytokines and T-cells. T-cells are lined with surface receptors that detect pathogens and elicit further immune responses, particularly toll-like receptor 4 (TLR4). TLR4 has been demonstrated to detect lipopolysaccharide (LPS), found on the outer membrane of Gram-negative bacteria. Recently, Basigin, a member of the immunoglobulin superfamily, has been shown to interact with TLR4 and is expressed on endothelial cells. The present study aims to address the expression pattern of Basigin and TLR4 in brain tissue stimulated with LPS for a variation of time to mirror acute and chronic inflammation, as well as different life stages to determine whether the expression pattern is dynamic. Total RNA and protein were purified from the isolated tissue and used in qRT-PCR and direct ELISA. The results of the study suggest expression of Basigin is elevated after 3 and 24 hours of incubation in LPS relative to control in adolescent mice, but not neonates. Expression of TLR4 did not change between age groups or incubation periods. The data suggest that expression of Basigin, but not TLR4, changes from neonate to adolescent age. This may leave the neonatal CNS more susceptible to an inflammatory response.

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