Medicine and Health Sciences Commons^™

Cell-Selective Knockout And 3d Confocal Image Analysis Reveals Separate Roles For Astrocyte- And Endothelial-Derived Ccl2 In Neuroinflammation, Debayon Paul, Shujun Ge, Yen Lemire, Evan R. Jellison, David R. Serwanski, Joel S. Pachter

UCHC Articles - Research

Background

Expression of chemokine CCL2 in the normal central nervous system (CNS) is nearly undetectable, but is significantly upregulated and drives neuroinflammation during experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis which is considered a contributing factor in the human disease. As astrocytes and brain microvascular endothelial cells (BMEC) forming the blood–brain barrier (BBB) are sources of CCL2 in EAE and other neuroinflammatory conditions, it is unclear if one or both CCL2 pools are critical to disease and by what mechanism(s).

Methods

Mice with selective CCL2 gene knockout (KO) in astrocytes (Astro KO) or …

Nf-Κb Contributes To The Detrimental Effects Of Social Isolation After Experimental Stroke, Venugopal Reddy Venna, Gillian Weston, Sharon E. Benashski, Sami Tarabishy, Fudong Liu, Jun Li, Lisa H. Conti, Louise D. Mccullough

UCHC Articles - Research

Social isolation (SI) is increasingly recognized as a risk factor for stroke. Individuals with lack of social support systems have an increased incidence of stroke, poorer recovery, and greater functional decline after injury compared to individuals with social support. Attesting to the importance of social factors in stroke outcome is that these same effects can be reproducibly demonstrated in animals; social interaction improves behavioral deficits and reduces damage after experimental stroke, whereas SI enhances injury. The mechanism by which SI exacerbates injury is unclear. We investigated the role of nuclear factor-kappaB (NF-κB) signaling in male mice that were pair housed …

Interleukin-1Β In Central Nervous System Injury And Repair, Nicole A. Jackman, Sandra J. Hewett, Robert J. Claycomb

UCHC Articles - Research

Acute inflammation is a self-limiting, complex biological response mounted to combat pathogen invasion, to protect against tissue damage, and to promote tissue repair should it occur. However, unabated inflammation can be deleterious and contribute to injury and pathology. Interleukin-1β (IL-1β), a prototypical “pro-inflammatory” cytokine, is essential to cellular defense and tissue repair in nearly all tissues. With respect to brain, however, studies suggest that IL-1β has pleiotrophic effects. It acts as a neuromodulator in the healthy central nervous system (CNS), has been implicated in the pathogenic processes associated with a number of CNS maladies, but may also provide protection to …