DOI: 10.1101/486589Dec 4, 2018Paper

Myeloid cell and transcriptome signatures associated with inflammation resolution in a model of self-limiting acute brain inflammation

BioRxiv : the Preprint Server for Biology
Claire L DaviesBarry W McColl

Abstract

Inflammation contributes to tissue repair and restoration of function after infection or injury. However, some forms of inflammation can cause tissue damage and disease, particularly if inappropriately activated, excessive, or not resolved adequately. The mechanisms that prevent excessive or chronic inflammation are therefore important to understand. This is particularly important in the central nervous system where some effects of inflammation can have particularly harmful consequences, including irreversible damage. An increasing number of neurological disorders, both acute and chronic, and their complications are associated with aberrant neuroinflammatory activity. Here we describe a model of self-limiting acute brain inflammation optimised to study mechanisms underlying inflammation resolution. Inflammation was induced by intracerebral injection of lipopolysaccharide (LPS) and the temporal profile of key cellular and molecular changes were defined during the progression of the inflammatory response. The kinetics of accumulation and loss of neutrophils in the brain enabled well demarcated phases of inflammation to be operatively defined, including induction and resolution phases. Microglial reactivity and accumulation of mon...Continue Reading

Related Concepts

Brain
Complication
Tissue Damage
Encephalitis
Gene Clusters
Gene Expression
Genes
Histocompatibility Antigens Class I
Inflammation
Chronic Inflammation

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