Modulation of inflammation and oxidative stress appears to limit sepsis-induced damage in experimental models.
The course of many diseases can be significantly improved by therapeutic modulation of inflammation.
Transplanted cells may improve function by local engraftment, trophic factors, or modulation of inflammation.
NAC would be interesting for testing whether the modulation of inflammation could correct tissue hypoxia during sepsis.
New therapeutic strategies based on modulation of inflammation, using mesenchymal stromal cells, miRNA, or regulatory T cells, have recently been proposed [6 8].
The putative effect of renal replacement therapy (RRT) on the prognosis of such patients is highly debated; some advocating that outcome might improve owing to modulation of inflammation.
The cytokines are significant in the modulation of inflammation through the process of cell signaling via autocrine, paracrine and endocrine signaling.
The current study aimed to elucidate the molecular mechanism, emphasizing the TLR signaling pathways in association with the potential recruitment of macrophages in the cochlea and the modulation of inflammation by ubiquitin-editing protein A20.
The role of specific proportions of ω-3 EPA and DHA, in the modulation of inflammation and oxidative stress markers associated to the progression of Metabolic Syndrome was investigated.
Experimental and clinical studies support a role for CRH, Ucn, Ucn2 and Ucn3 in the endocrine/immune modulation of inflammation in human trophoblast; however the intracellular mechanisms are not yet recognized.
Modulation of inflammation appears to be the major mechanism behind HO-1 cytoprotection.
