Ashley M Ingiosi

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The reciprocal interactions between sleep and immune function are well-studied. Insufficient sleep induces innate immune responses as evidenced by increased expression of pro-inflammatory mediators in the brain and periphery. Conversely, immune challenges upregulate immunomodulator expression, which alters central nervous system-mediated processes and(More)
Sleep-wake behavior is altered in response to immune challenge. Although the precise mechanisms that govern sickness-induced changes in sleep are not fully understood, interleukin-1β (IL-1) is one mediator of these responses. To better understand mechanisms underlying sleep and inflammatory responses to immune challenge, we used two transgenic mouse strains(More)
Interactions between sleep and immune function are bidirectional. Although the mechanisms that govern these interactions are not fully elucidated, the pro-inflammatory cytokine, interleukin-1β (IL-1), is a known regulator of sleep and mediator of immune responses. To further clarify the underlying substrates of sleep and immune interactions, we engineered(More)
Sepsis is a systemic immune response to infection that may result in multiple organ failure and death. Polymicrobial infections remain a serious clinical problem, and in the hospital sepsis is the number one non-cardiac killer. Although the central nervous system may be one of the first systems affected, relatively little effort has been made to determine(More)
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