Thrombin induces the expression of oncostatin M via AP-1 activation in human macrophages: a link between coagulation and inflammation.

Macrophages as inflammatory cells are involved in the pathogenesis of atherosclerosis that today is recognized as an inflammatory disease. Activation of coagulation leads to the late complication of atherosclerosis, namely atherothrombosis with its clinical manifestations stroke, unstable angina, myocardial infarction, and sudden cardiac death. Thus inflammation and coagulation play fundamental roles in the pathogenesis of atherosclerosis.

In human macrophages the complement component C5a induces the expression of oncostatin M via AP-1 activation.

Objective: Macrophages produce the cytokine oncostatin M (OSM), which beside other functions is also involved in inflammation. The complement component C5a mobilizes and activates these cells at inflammatory sites. We examined the effect of C5a on OSM production in human monocytes and in human monocyte-derived macrophages.

The complement component C5a induces the expression of plasminogen activator inhibitor-1 in human macrophages via NF-kappaB activation.

Background: Atherosclerosis is considered to be a chronic inflammatory disorder. Activation of the complement cascade is a major aspect of chronic inflammatory diseases. Complement components were identified in atherosclerotic plaques, and a correlation between adverse events and C5a plasma levels was found.

Treatment of type I diabetic with subcutaneous insulin resistance by a totally implantable insulin infusion device ("Infusaid").

A 22-yr-old diabetic female is described who developed insulin resistance due to subcutaneous (and intramuscular) "malabsorption" of insulin resulting in recurrent ketoacidosis and sepsis. Intravenous insulin sensitivity was maintained. Diverse attempts to prevent metabolic decompensation by "external" methods failed.