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      Modulation of Polymorphonuclear Leukocyte Apoptosis in the Critically Ill by Removal of Cytokines with Continuous Hemodiafiltration

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          Delay of polymorphonuclear leukocyte (PMN) apoptosis caused by hypercytokinemia is considered to be a potential cause of tissue damage and resultant organ failure. We evaluated whether continuous hemodiafiltration using a polymethylmethacrylate membrane hemofilter (PMMA-CHDF), which can remove cytokines in the circulating blood, can modulate apoptosis in peripheral blood neutrophils and thereby reduce tissue damage and organ dysfunction in 25 critically ill patients. Following the completion of a 3-day PMMA-CHDF session, serum cytokine levels were significantly decreased and the percentage of apoptotic PMNs was significantly increased. A significant correlation was observed between the PMMA-CHDF-induced increase in the percentage of apoptotic PMNs and the degree of decrease in the serum interleukin-6 level. A significant correlation was also found between the increase in the percentage of apoptotic PMNs and improvement in sequential organ failure assessment score following PMMA-CHDF. These results suggest that PMMA-CHDF in critically ill patients with hypercytokinemia and concomitant delay in apoptosis of PMNs can alleviate the delay of PMN apoptosis through the removal of serum cytokines and thus may result in avoidance of organ dysfunction.

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          Most cited references 6

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          Inflammatory cytokines and cell response in surgery.

          The systemic inflammatory response as mediated by the cytokine network is undoubtedly complex. While inflammatory cytokines are indispensable in wound healing and the restoration of homeostasis, it is often the excessive activity of either proinflammatory or anti-inflammatory cytokines that causes injury to the host or renders the host immunocompromised, respectively. Central to the functional biology of cytokines in surgical injury and infections are the responses of immune cells to such insults. It is clear that immunocytes are the source of cytokine production, and these products possess important autocrine, as well as systemic activities. The ability to alter immunocyte function through extracellular hormonal influences or by manipulating intracellular signaling mechanisms are potential strategies for regulating the inflammatory cytokine response during injury.
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            Poly's lament: the neglected role of the polymorphonuclear neutrophil in the afferent limb of the immune response.

            The polymorphonuclear leucocyte (PMN) has traditionally been thought to participate in the inflammatory response only as an effector cell. However, recent data demonstrate that PMNs can synthesize and release cytokines, such as IL-1, TNF-alpha and IL-6, and hence modulate both T- and B-cell activities in the evolution of an immune response.
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              The role of cytokines and adhesion molecules in the development of inflammatory injury.

              Clinicians are constantly challenged by patients who demonstrate the ill effects of an uncontrolled host inflammatory response. Patients with sepsis and adult respiratory distress syndrome (ARDS) are frequently encountered examples of this syndrome. Despite advances in intensive care, mortality from these syndromes remains unchanged over the past two decades. In order to gain a better understanding of this pathophysiological response and to identify more specific therapeutic targets, the techniques of molecular biology have been applied to in vivo inflammatory models. Recent data indicate that the inflammatory response is dependent on the presence of both cytokines and adhesion molecules that mediate neutrophil-endothelial cell adhesive interactions. In this article, we review our experience using a lung model of inflammation that has provided insight into the events leading to injury. Cytokines [particularly, interleukin 1 (IL-1) and tumor necrosis factor alpha (TNF-alpha)], and endothelial, as well as leukocyte, adhesion molecules appear to coordinate a cascade of interactions between leukocytes and endothelial cells, which results in tissue injury.

                Author and article information

                Blood Purif
                Blood Purification
                S. Karger AG
                July 2004
                30 March 2004
                : 22
                : 2
                : 188-197
                aDepartment of Emergency and Critical Care Medicine, Graduate School of Medicine, Chiba University, bDivision of Blood Transfusion, Chiba University Hospital, and cDepartment of Emergency and Critical Care Medicine, Kimitsu Cyuou Hospital, Chiba, Japan
                76852 Blood Purif 2004;22:188–197
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 7, Tables: 1, References: 42, Pages: 10
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/76852
                Original Paper


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