Cytokine
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TREM-1 is an activating receptor expressed on the surface of neutrophils and mature monocytes when stimulated by bacteria or fungi, leading to amplification of the inflammatory response. Our objective is to analyze the prognostic value of serum sTREM-1 levels and other mediators of the inflammatory response, in patients hospitalized for CAP, and to compare its prognostic value with those of advanced age, pneumonia severity scores, Charlson index, nutritional status and severity of sepsis. ⋯ This study confirms the usefulness of TREM-1 in the diagnosis and prognosis of patients with CAP, which is independent of advanced age, other inflammation markers such as IL-6, severity index for CAP such as CURB-65 or PSI, severity of sepsis and nutritional status including IGF-1.
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Multiple pro-inflammatory mediators contribute to cardiac dysfunction caused by bacterial lipopolysaccharide (LPS). The rapid TNF-alpha response is likely involved in the induction of down-stream myocardial depressant factors. Studies by our laboratory and others indicate an important role for ICAM-1 in endotoxemic cardiac dysfunction through leukocyte-independent mechanisms. The purpose of this study was to determine: whether ICAM-1 knockout improves cardiac function during endotoxemia and whether TLR4 and TNF-alpha regulate LPS-induced myocardial ICAM-1 expression. ⋯ ICAM-1 contributes to the mechanism of endotoxemic cardiac dysfunction. TNF-alpha is involved in the regulation of myocardial ICAM-1 expression by TLR4.