TY - JOUR
T1 - The yin/yang of inflammatory status
T2 - Blood-brain barrier regulation during sleep
AU - Hurtado-Alvarado, G.
AU - Becerril-Villanueva, E.
AU - Contis-Montes de Oca, A.
AU - Domínguez-Salazar, E.
AU - Salinas-Jazmín, N.
AU - Pérez-Tapia, S. M.
AU - Pavon, L.
AU - Velázquez-Moctezuma, J.
AU - Gómez-González, B.
N1 - Publisher Copyright:
© 2017 Elsevier Inc.
PY - 2018/3
Y1 - 2018/3
N2 - Sleep loss induces a low-grade inflammatory status characterized by a subtle but sustained increase of pro-inflammatory mediators, which are key regulators of blood-brain barrier function. To investigate the influence of inflammatory status on blood-brain barrier dysfunction induced by sleep restriction we performed an experiment using two strains of mice with different immunological backgrounds, C57BL/6 mice that have a predominant pro-inflammatory response and BALB/c mice that have a predominant anti-inflammatory response. Mice were sleep-restricted during 10 days using the flowerpot technique during 20 h per day with 4 h of daily sleep opportunity. The systemic inflammatory status, blood-brain barrier permeability, and the hippocampal expression of neuroinflammatory markers were characterized at the 10th day. Serum levels of TNF and IFN-γ increased in sleep-restricted C57BL/6 but not in BALB/c mice; no changes in other cytokines were found. Sleep restriction increased blood-brain barrier permeability in C57BL/6 strain but not in BALB/c. The hippocampus of sleep-restricted C57BL/6 mice exhibited an increase in the expression of the neuroinflammatory markers Iba-1, A 2A adenosine receptor, and MMP-9; meanwhile in sleep-restricted BALB/c mice the expression of this markers was lesser than the control group. These data suggest that cytokines may be playing a key role in modulating blood-brain barrier function during sleep restriction, and probably the effects are related to Iba-1, MMP-9 and A 2A adenosine receptor overexpression.
AB - Sleep loss induces a low-grade inflammatory status characterized by a subtle but sustained increase of pro-inflammatory mediators, which are key regulators of blood-brain barrier function. To investigate the influence of inflammatory status on blood-brain barrier dysfunction induced by sleep restriction we performed an experiment using two strains of mice with different immunological backgrounds, C57BL/6 mice that have a predominant pro-inflammatory response and BALB/c mice that have a predominant anti-inflammatory response. Mice were sleep-restricted during 10 days using the flowerpot technique during 20 h per day with 4 h of daily sleep opportunity. The systemic inflammatory status, blood-brain barrier permeability, and the hippocampal expression of neuroinflammatory markers were characterized at the 10th day. Serum levels of TNF and IFN-γ increased in sleep-restricted C57BL/6 but not in BALB/c mice; no changes in other cytokines were found. Sleep restriction increased blood-brain barrier permeability in C57BL/6 strain but not in BALB/c. The hippocampus of sleep-restricted C57BL/6 mice exhibited an increase in the expression of the neuroinflammatory markers Iba-1, A 2A adenosine receptor, and MMP-9; meanwhile in sleep-restricted BALB/c mice the expression of this markers was lesser than the control group. These data suggest that cytokines may be playing a key role in modulating blood-brain barrier function during sleep restriction, and probably the effects are related to Iba-1, MMP-9 and A 2A adenosine receptor overexpression.
KW - A adenosine receptor
KW - BALB/c
KW - Blood-brain barrier
KW - C57BL/6
KW - CBA array
KW - Iba-1
KW - MMP-9
KW - Neuroinflammation
KW - Sleep restriction
UR - http://www.scopus.com/inward/record.url?scp=85034840800&partnerID=8YFLogxK
U2 - 10.1016/j.bbi.2017.11.009
DO - 10.1016/j.bbi.2017.11.009
M3 - Artículo
C2 - 29154957
SN - 0889-1591
VL - 69
SP - 154
EP - 166
JO - Brain, Behavior, and Immunity
JF - Brain, Behavior, and Immunity
ER -