Blocking toll-like receptor 2 and 4 signaling during a stressor prevents stress-induced priming of neuroinflammatory responses to a subsequent immune challenge

Highlight • Antagonism of TLR2 and TLR4 during a stressor abrogated the stress-induced sensitized neuroinflammatory response to an immune challenge.

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Bibliographische Detailangaben
Veröffentlicht in:	Brain, behavior, and immunity behavior, and immunity, 2013-08, Vol.32, p.112-121
Hauptverfasser:	Weber, Michael D, Frank, Matthew G, Sobesky, Julia L, Watkins, Linda R, Maier, Steven F
Format:	Artikel
Sprache:	eng
Schlagworte:	Allergy and Immunology Animals Cisterna Magna Cytokine Cytokines - biosynthesis Cytokines - genetics Electroshock Hippocampus - pathology Immunity, Innate Inflammation - pathology Injections Interleukin-1beta - biosynthesis Interleukin-1beta - genetics Lipopolysaccharides - pharmacology Male Microglia Neuroimmunomodulation - drug effects Neuroinflammation Phosphatidylcholines - pharmacology Priming Psychiatry Rats Rats, Sprague-Dawley Real-Time Polymerase Chain Reaction Stress Stress, Psychological - immunology Stress, Psychological - pathology Toll-like receptor Toll-Like Receptor 2 - antagonists & inhibitors Toll-Like Receptor 4 - antagonists & inhibitors
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Beschreibung
Zusammenfassung:	Highlight • Antagonism of TLR2 and TLR4 during a stressor abrogated the stress-induced sensitized neuroinflammatory response to an immune challenge.
ISSN:	0889-1591 1090-2139
DOI:	10.1016/j.bbi.2013.03.004