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Synergistic effects of NOD1 or NOD2 and TLR4 activation on mouse sickness behavior in relation to immune and brain activity markers.

Farzi A, Reichmann F, Meinitzer A, Mayerhofer R, Jain P, Hassan AM, Fröhlich EE, Wagner K, Painsipp E, Rinner B, Holzer P - Brain Behav. Immun. (2014)

Bottom Line: Intraperitoneal injection of FK565 (0.001 or 0.003mg/kg) or MDP (1 or 3mg/kg) 4h before LPS (0.1 or 0.83mg/kg) significantly aggravated and prolonged the LPS-evoked sickness behavior as deduced from a decrease in locomotion, exploration, food intake and temperature.When given alone, FK565 and MDP had only minor effects.Immunohistochemical visualization of c-Fos in the brain revealed that NOD2 synergism with TLR4 resulted in increased activation of cerebral nuclei relevant to sickness.

View Article: PubMed Central - PubMed

Affiliation: Research Unit of Translational Neurogastroenterology, Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Universitätsplatz 4, 8010 Graz, Austria. Electronic address: aitak.farzi@medunigraz.at.

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Effects of MDP (3 mg/kg), FK565 (0.003 mg/kg) and LPS (0.1 mg/kg) on circulating corticosterone (CORT) levels 3 h (A) and 26 h (B) after treatment, as well as on the kynurenine/tryptophan (KYN/TRP) ratio (C) and circulating levels of kynurenine (D) and tryptophan (E) measured 26 h after treatment of male mice. Plasma CORT was measured 3 h after treatment (A) and 26 h after treatment, 30 min following exposure to tail suspension stress (B). Likewise, plasma kynurenine and tryptophan (C–E) were determined 26 h after treatment, 30 min following exposure to tail suspension stress. The values are means + SEM, n = 7–8. (A): Main factor effects without NOD × LPS interactions: ap < 0.001, LPS versus VEH. bp < 0.001, FK565 versus VEH or MDP. (B–E): One-way ANOVA: +p < 0.1, ∗p < 0.05, ∗∗p < 0.01, versus VEH or as indicated by the brackets.
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f0035: Effects of MDP (3 mg/kg), FK565 (0.003 mg/kg) and LPS (0.1 mg/kg) on circulating corticosterone (CORT) levels 3 h (A) and 26 h (B) after treatment, as well as on the kynurenine/tryptophan (KYN/TRP) ratio (C) and circulating levels of kynurenine (D) and tryptophan (E) measured 26 h after treatment of male mice. Plasma CORT was measured 3 h after treatment (A) and 26 h after treatment, 30 min following exposure to tail suspension stress (B). Likewise, plasma kynurenine and tryptophan (C–E) were determined 26 h after treatment, 30 min following exposure to tail suspension stress. The values are means + SEM, n = 7–8. (A): Main factor effects without NOD × LPS interactions: ap < 0.001, LPS versus VEH. bp < 0.001, FK565 versus VEH or MDP. (B–E): One-way ANOVA: +p < 0.1, ∗p < 0.05, ∗∗p < 0.01, versus VEH or as indicated by the brackets.

Mentions: The PRR agonists under study had a distinct effect to enhance the plasma levels of corticosterone as measured 3 h after injection. Two-way ANOVA revealed a significant main factor effect for LPS (F(1,40) = 76.581, p < 0.001) and the NOD agonists (F(2,40) = 16.608, p < 0.001) without a significant interaction. Post-hoc analysis of the main factor effects disclosed that FK565 increased circulating corticosterone compared to VEH and MDP (Fig. 7A).


Synergistic effects of NOD1 or NOD2 and TLR4 activation on mouse sickness behavior in relation to immune and brain activity markers.

Farzi A, Reichmann F, Meinitzer A, Mayerhofer R, Jain P, Hassan AM, Fröhlich EE, Wagner K, Painsipp E, Rinner B, Holzer P - Brain Behav. Immun. (2014)

Effects of MDP (3 mg/kg), FK565 (0.003 mg/kg) and LPS (0.1 mg/kg) on circulating corticosterone (CORT) levels 3 h (A) and 26 h (B) after treatment, as well as on the kynurenine/tryptophan (KYN/TRP) ratio (C) and circulating levels of kynurenine (D) and tryptophan (E) measured 26 h after treatment of male mice. Plasma CORT was measured 3 h after treatment (A) and 26 h after treatment, 30 min following exposure to tail suspension stress (B). Likewise, plasma kynurenine and tryptophan (C–E) were determined 26 h after treatment, 30 min following exposure to tail suspension stress. The values are means + SEM, n = 7–8. (A): Main factor effects without NOD × LPS interactions: ap < 0.001, LPS versus VEH. bp < 0.001, FK565 versus VEH or MDP. (B–E): One-way ANOVA: +p < 0.1, ∗p < 0.05, ∗∗p < 0.01, versus VEH or as indicated by the brackets.
© Copyright Policy - CC BY
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4295938&req=5

f0035: Effects of MDP (3 mg/kg), FK565 (0.003 mg/kg) and LPS (0.1 mg/kg) on circulating corticosterone (CORT) levels 3 h (A) and 26 h (B) after treatment, as well as on the kynurenine/tryptophan (KYN/TRP) ratio (C) and circulating levels of kynurenine (D) and tryptophan (E) measured 26 h after treatment of male mice. Plasma CORT was measured 3 h after treatment (A) and 26 h after treatment, 30 min following exposure to tail suspension stress (B). Likewise, plasma kynurenine and tryptophan (C–E) were determined 26 h after treatment, 30 min following exposure to tail suspension stress. The values are means + SEM, n = 7–8. (A): Main factor effects without NOD × LPS interactions: ap < 0.001, LPS versus VEH. bp < 0.001, FK565 versus VEH or MDP. (B–E): One-way ANOVA: +p < 0.1, ∗p < 0.05, ∗∗p < 0.01, versus VEH or as indicated by the brackets.
Mentions: The PRR agonists under study had a distinct effect to enhance the plasma levels of corticosterone as measured 3 h after injection. Two-way ANOVA revealed a significant main factor effect for LPS (F(1,40) = 76.581, p < 0.001) and the NOD agonists (F(2,40) = 16.608, p < 0.001) without a significant interaction. Post-hoc analysis of the main factor effects disclosed that FK565 increased circulating corticosterone compared to VEH and MDP (Fig. 7A).

Bottom Line: Intraperitoneal injection of FK565 (0.001 or 0.003mg/kg) or MDP (1 or 3mg/kg) 4h before LPS (0.1 or 0.83mg/kg) significantly aggravated and prolonged the LPS-evoked sickness behavior as deduced from a decrease in locomotion, exploration, food intake and temperature.When given alone, FK565 and MDP had only minor effects.Immunohistochemical visualization of c-Fos in the brain revealed that NOD2 synergism with TLR4 resulted in increased activation of cerebral nuclei relevant to sickness.

View Article: PubMed Central - PubMed

Affiliation: Research Unit of Translational Neurogastroenterology, Institute of Experimental and Clinical Pharmacology, Medical University of Graz, Universitätsplatz 4, 8010 Graz, Austria. Electronic address: aitak.farzi@medunigraz.at.

Show MeSH
Related in: MedlinePlus