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Thrombin, Inflammation, and Cardiovascular Disease: Inflammatory cytokines

The exact mechanism for the association of CRP with coagulation status is not clear; however the work of Ritchie and colleagues suggests a possible pathway. Monocytes appear capable of binding FDPs and subsequently producing IL-6, which goes to the liver and affects the wide range of proteins known to be in the acute-phase response. This has been proposed to be the mechanism by which fibrinogen consumption is replaced, and may be an important mechanism connecting coagulation and inflammation. This theory may have far-reaching implications both in the general biology we have been discussing and in such areas as drug development, where the coagulation-inflammation connection in sepsis, as described by Esmon et al, has been recently exploited. Reading here

Adipose tissue is a key producer of inflammatory cytokines (so-called “adipokines”), among which IL-6 is a major pathophysiologic mediator of diabetes and the metabolic syndrome, as well as acute-phase proteins, such as CRP. In this way, the metabolic syndrome may be a contributor to inflammatory response through the visceral obesity component: increased visceral fat may lead to increased proinflammatory response to a variety of stimulants, resulting in a chronic up-regulation of IL-6 production. Chronic up-regulation of IL-6 may predispose a patient to atherosclerosis in a number of ways. We have demonstrated in murine atherosclerosis that chronic injections of small amounts of IL-6 (yielding a minor chronic acute-phase response) resulted in a twofold to fivefold increase in lesion size. In humans, IL-6 activities range from acute-phase response to tissue factor expression by monocytes, and many others.
The association of CRP with insulin level is at least partially independent of adiposity, and is strongly related to insulin sensitivity.