Age exacerbates sickness behavior following exposure to a viral mimetic
Kristina A McLinden1, Dinko Kranjac, Lauren E Deodati
1Department of Psychology, Texas Christian University, Ft. Worth, TX 76129, USA.
Abstract:
Poly I:C, a viral mimetic, is a synthetic double-stranded RNA that is known to cause activation of the innate immune system, resulting in the emergence of sickness behaviors in otherwise healthy adult mice. However, the way in which such effects of poly I:C manifest themselves in aged mice are not currently known. We hypothesized that poly I:C administration would lead to burrowing deficits, but that these deficits would be exaggerated in aged subjects (19-months old) compared to young subjects (4-months old) that received the same dose. In order to associate these behavioral decrements with inflammatory factors, we measured mRNA expression of IL-1β and IL-6 in the hippocampus and parietal cortex and peripheral protein expression of IL-6, TNF-α, MCP-1, MIP-1α, and IL-1β in the serum. After exposure to poly I:C, aged subjects demonstrated significant impairments in their burrowing behavior, compared to younger subjects administered the same dose. These behavioral decrements coincided with increased expression of IL-6 among animals exposed to poly I:C and increased expression of IL-1β among aged animals in the hippocampus and cortex. Furthermore, we observed an increase in peripheral poly I:C-induced IL-6, TNF-α, MCP-1, and MIP-1α, but not IL-1β. These results indicate that virus-mediated immune activation in the aging body can lead to increased sickness behavior. Furthermore, these data indicated a possible dissociation between the effects of poly I:C on sickness behaviors in aged mice, with central expression of IL-1β potentially playing a role in age-related impairments.
Insights
Poly I:C, a viral mimetic, exacerbates sickness behaviors in aged mice, causing significant burrowing deficits. These impairments correlate with increased central and peripheral inflammatory markers, highlighting age-related immune system vulnerabilities.
Area of Science:
- Immunology
- Neuroscience
- Aging Research
Background:
- Polyriboinosinic:polyribouridilic acid (Poly I:C) activates the innate immune system, inducing sickness behaviors in adult mice.
- The impact of Poly I:C on sickness behaviors in aged mice remains largely unknown.
- Aging is associated with altered immune responses and increased susceptibility to inflammatory conditions.
Purpose of the Study:
- To investigate the effects of Poly I:C on sickness behaviors in aged mice compared to young mice.
- To determine if Poly I:C-induced behavioral deficits in aged mice are associated with changes in inflammatory gene and protein expression.
- To explore potential age-related differences in the central and peripheral inflammatory responses to Poly I:C.
Main Methods:
- Administration of Poly I:C to young (4-month-old) and aged (19-month-old) mice.
- Assessment of burrowing behavior as a measure of sickness behavior.
- Quantification of mRNA expression for IL-1β and IL-6 in hippocampal and parietal cortex tissues.
- Measurement of peripheral serum protein levels for IL-6, TNF-α, MCP-1, MIP-1α, and IL-1β.
Main Results:
- Aged mice exhibited significantly greater burrowing deficits after Poly I:C administration compared to young mice.
- Poly I:C exposure increased IL-6 expression in both young and aged mice.
- Aged mice showed increased IL-1β expression in the hippocampus and cortex following Poly I:C treatment.
- Peripheral levels of IL-6, TNF-α, MCP-1, and MIP-1α were elevated by Poly I:C, but IL-1β did not significantly change in the serum.
- A potential dissociation between central and peripheral inflammatory responses and sickness behavior was observed in aged mice.
Conclusions:
- Poly I:C administration leads to exaggerated sickness behaviors in aged mice, suggesting heightened immune system sensitivity.
- Increased central IL-1β expression in aged mice may contribute to age-related impairments in sickness behavior.
- These findings underscore the impact of virus-mediated immune activation on sickness behavior in the aging population and highlight age-specific inflammatory mechanisms.
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