The plasma concentration of sCD146 is modulated in inflammatory diseases associated with endothelial alterations (Bardin et al, 2006).
The observations that both IL-6 and claudin 2 may be modulated in both human and murine inflammatory disease of the intestine suggest that this relationship could be of importance in the pathogenesis of inflammatory bowel disease.
The acute-phase protein response may contribute to muscle wasting, as it is modulated in part by pro-inflammatory cytokines: IL-1, IL-6, TNF- α, IFN- γ (McNamara et al, 1992).
Hepcidin expression is modulated in response to infectious and inflammatory stimuli [ 14, 17].
Even greater challenges exist for the more complex glycosylation events observed extracellularly, which are employed in cell cell communication and cell recognition and are modulated in several diseases, including cancers, inflammatory diseases, and bacterial and viral infections.
Previous studies have shown that sCD146 is detectable in the human blood and its level is modulated in different pathologies, such as inflammatory bowel diseases, vasculitis, pathologic pregnancies and chronic renal failure (Bardin et al, 2003; Pasquier et al, 2005; Bardin et al, 2006).
The secretory profile of these inflammatory markers was modulated in co-cultures of both cell types.
The inflammatory response is modulated in part by a bidirectional communication between the brain and the immune systems.
The systemic inflammatory response is highly complex and is modulated, in part, by the interaction of pro- and anti-inflammatory cytokines.
As revealed through network analysis, inflammatory response pathways were modulated in lung cells exposed to air pollutants.
