An investigation into inflammatory cytokine secretion in THP-1 Derived Microglia
Cardiff Metropolitan University
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The enormous cost and social burden of neuro-inflammatory diseases presents an urgent requirement for treatment and prevention of their development. Microglial cells, the macrophages of the central nervous system (CNS), are the first and main line of defence against pathogens of the CNS and therefore microglial cell models are extremely sort after in order to develop a better understanding of the pathogenesis of neuro-degenerative disease. It is apparent that in the early stages of many neuro-inflammatory diseases, such as stroke, the protective blood brain barrier (BBB) that encompasses the CNS becomes much more plastic allowing an influx of circulating peripheral monocytes into the immune privileged site. It is therefore unsurprising that evidence exists to support the theory of cross talk between peripheral and neural inflammation. For example, in the elderly, systemic infection is associated with an increased frequency of behavioural and cognitive complications. With studies proving beneficial macrophage polarization can be maintained in the anti-inflammatory state, modulation partly in the circulation may be transferable to the CNS thus helping to manage neurodegenerative disease. The development of a microglial like-cellular model based on human monocytes has a huge potential for studying cellular mechanisms, particularity inflammation. This study aimed to investigate the effect of LPS on the secretion of three inflammatory cytokines in a THP-1 derived microglial model using monocytes as a control. During the study THP-1 cells were transformed into a microglial-like cell line and treated with 3 different concentrations of lipopolysaccharide (1g, 0.1g, 0.01g) and incubated for 6 hours. The supernatants IL-1, IL-6 and TNF were collected and quantified by means of ELISA. Results showed significant levels of the cytokines IL-1 and TNF secreted in particular after incubation with the lower concentrations of LPS, but no detectable levels of IL-6, thus disproving the hypothesis that the higher concentration of LPS would induce higher secretions of the inflammatory cytokines. future studies are required to fully investigate the elusive inflammatory mechanisms of these cells.
BSc (Hons) Biomedical Science
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