AI Article Synopsis
- The study examined mRNA expression of PTX3 and PK11195 binding in the spinal cords of Lewis rats with induced EAE, finding PTX3 levels spiking during active disease and persisting for an extended period.
- Elevated TNF and IL-6 levels corresponded with the disease onset but returned to normal by days 14-17, indicating a more temporary inflammatory response.
- Treatments like dexamethasone suppressed all changes, while rolipram delayed the disease's onset and severity but did not reduce the eventual inflammatory peaks of TNF, IL-6, PTX3, or PK11195.
Article Abstract
We have studied the mRNA expression of pentraxin 3 (PTX3) and the binding of the peripheral-type benzodiazepine receptor (PBR) ligand, [3H]-PK11195, in the spinal cord of Lewis rats where EAE was actively induced. PTX3 was induced during the active phase of EAE (day 10-14), it remained high up to 30 days and disappeared only 60 days later. Similarly, PK11195 binding peaked at day 14-17 during the recovery and it disappeared by day 60. On the other hand, the levels of TNF and IL-6 in the spinal cord were elevated at the peak and at the onset of clinical signs and returned to non-detectable by day 14-17. Dexamethasone abolished all these changes, while treatment with rolipram, delayed the appearance of the disease and then decreased its severity. However the peaks of TNF, IL-6, PBR and PTX3 levels in spinal cord were only delayed, but not reduced, by rolipram treatment. In conclusion, we show two types of inflammatory changes in EAE: acute, short term changes (TNF and IL-6), that correlate with the disease; and effects such as PTX3 expression and PK11195 binding that last longer after recovery from the disease.
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| http://dx.doi.org/10.1016/s0165-5728(00)00279-4 | DOI Listing |
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