Aspects of the pathophysiological steps leading to preterm labor after intrauterine infection can be studied in a cell culture model of decidua-derived cells. In this model, bradykinin (BK) increases the release of arachidonic acid (AA), the precursor of labor-promoting prostaglandins. The release is more than additively increased when cells are pretreated with interleukin-1beta (IL-1beta). Binding studies indicate that the expression of the bradykinin B2-receptor (B2R) protein rises to up to 300% of control after incubation with IL-1beta for 24 h. Thus, there is an increased capacity of mediating the response to BK. These findings suggest a pivotal role for the kallikrein-kinin system (KKS) during labor caused by intrauterine infection. However, there was no binding to the bradykinin B1-receptor (B1R), and it could not be induced by IL-1R, which is a unique finding compared with other cell systems.
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