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Poly adenosine diphosphate (ADP) ribose polymerase (PARP) activity is known to modulate inflammation in animal models of injury.
Besides driving the propagation of pain signals, spinal mechanisms are also discussed to modulate inflammation in the periphery.
The aims of this study were to modulate inflammation in synovial explants with the compounds: dexamethasone, rapamycin, bone morphogenetic protein 7 (BMP-7) and pravastatin, and to investigate the modulatory capacity of the compounds on specific macrophage phenotypes.
These findings open a new line for further investigations which could result in a new way to modulate inflammation in chronic migraine.
In summary, this study shows that HSP70 can modulate inflammation in a model for chronic and progressive arthritis through IL-10 dependent mechanisms, operating via suppression of pathogenic antibody responses and the development of regulatory T cells.
Importantly, intracerebroventricular administered palmitoylethanolamide failed to modulate inflammation in PPARα knockout mice.
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Maiuri, L. et al. Tissue transglutaminase activation modulates inflammation in cystic fibrosis via PPARγ down-regulation.
Frasnelli, M. E., Tarussio, D., Chobaz-péclat, V., Busso, N. & So, A. TLR2 modulates inflammation in zymosan-induced arthritis in mice.
Surfactant protein D (SP-D) mediates clearance of microorganisms and modulates inflammation in response to cytotoxic stimulation.
Knowing the mechanisms how monocytes can be turned into anti-inflammatory cells will allow for targeted therapeutic intervention using these pathways to down-modulate inflammation in vivo.
Taken together our data reveal that enteric neurons producing NPY play an important role in modulating inflammation in colitis.
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