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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: Escalating morphine dosing in HIV-1 Tat transgenic mice with sustained Tat exposure reveals an allostatic shift in neuroinflammatory regulation accompanied by increased neuroprotective non-endocannabinoid lipid signaling molecules and amino acids

Fig. 5

Cytokine concentrations (pg/mL) are impacted by Tat exposure and morphine in the striatum (a) and spinal cord (b) of Tat transgenic mice. Proinflammatory cytokines showed morphine- and Tat-specific effects in the striatum and spinal cord. Morphine treatment led to a significant increase in multiple proinflammatory cytokines in the striatum (IL-1α, IL-9, IL-12p70) and spinal cord (IL-9, IL-12p70, IL-17A), while reducing IL-1β in the spinal cord. Tat exposure reduced several cytokines in the striatum (IL-1α, IL-17A) and spinal cord (IL-3). Morphine and Tat interactions were noted for IL-3 and IL-12p40 in the striatum. Anti-inflammatory cytokine IL-10 (highlighted, bottom right) was elevated by morphine in the spinal cord and reduced by Tat expression in the striatum, whereas IL-4 indicated a significant morphine by Tat interaction for both CNS regions. All data are expressed as mean pg/mL ± SEM. Samples were normalized to 900 μg/mL (striatum) or 500 μg/mL (spinal cord) via BCA. Statistical significance was assessed by ANOVA followed by Tukey’s post hoc test; *p < 0.05 main effect of drug; #p < 0.05 main effect of genotype; p < 0.05 vs. morphine-exposed Tat(−) mice; §p < 0.05 vs. morphine-exposed Tat(+) mice. Morph short-term (8-day) morphine injections. n = 5–6 mice per group

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