Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004610 (bacteremia)
 13,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of CD11b (CR3, complement receptor type three), CD16 (FcR, Fc IgG receptor), and CD35 (CR1, complement receptor type one) on neutrophils obtained from thermally injured patients was examined using immunofluorescence and flow cytometry. Because defects in neutrophil function have been related to an increased risk of infection and death following thermal injury, we compared changes in neutrophil subpopulations following thermal injury with the onset of infection. Neutrophils from 34 patients with large thermal injuries were monitored weekly for CD11, CD16, and CD35. Changes in the cell surface antigens over time were compared with the incidence of bacteremia and pneumonia. Although the percentages of CD16+ CD11+ neutrophils were suppressed in almost all patients, the changes which occur in each individual patient rather than the actual values appear to be of major importance. Patients developing bacteremia or pneumonia displayed a significant reduction in both the percentage and absolute number of CD16+ CD11+ neutrophils compared to their preinfection values. The values did not increase until the infections were completely cleared. Patients remaining free of bacteremia or pneumonia usually had lower than normal percentages of CD16+ and CD11+ neutrophils with no predictable pattern being noted. The percentage of CD35+ neutrophils dropped within 1 week following thermal injury in all patients but did not correlate with the onset of infections.
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PMID:Flow cytometric analysis of neutrophil subsets in thermally injured patients developing infection. 196 60

Kupffer cells are well known to be important for normal host defense function. The development of methods to evaluate the in vivo function of specific receptors on Kupffer cells has made it possible to assess the role of these receptors in host defense. The rationale for studying complement receptors is based on the proposed important role of these receptors in host defense and on the observation that the hereditary deficiency of a complement receptor is associated with recurrent severe bacterial infections. The studies reviewed here demonstrate that forms of injury that are associated with depressed host defense including thermal injury, hemorrhagic shock, trauma, and surgery also cause a decrease in complement receptor clearance function. This decrease in Kupffer cell receptor clearance function was shown not to be the result of depressed hepatic blood flow or depletion of complement components. Complement receptor function was also depressed following the phagocytosis of particulates that are known to depress Kupffer cell host defense function. Endotoxemia and bacteremia also were associated with a depression of complement receptor function. Complement receptor function was experimentally depressed in uninjured animals by the phagocytosis of IgG-coated erythrocytes. There was a close association between the depression of complement receptor clearance function and increased susceptibility to the lethal effects of endotoxin and bacterial infection. These studies support the hypotheses that complement receptors on Kupffer cells are important for normal host defense and that depression of the function of these receptors impairs host defense.
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PMID:Kupffer cell complement receptor clearance function and host defense. 353 89

The phagocytosis of erythrocytes by macrophages has previously been shown to depress macrophage function. In this study we compared the effect of the phagocytosis of erythrocytes and erythrocyte ghosts by Kupffer cells on the duration of the depression of complement receptor clearance function and host defense against endotoxemia and bacteremia. Phagocytosis of erythrocytes and erythrocyte ghosts was induced in rats by the injection of rat erythrocytes or erythrocyte ghosts coated with anti-rat erythrocyte immunoglobulin G (EIgG and GIgG, respectively). The hepatic uptake of EIgG and GIgG (17.4 X 10(8)/100 g) occurred during the first 30 min after injection. The digestion of phagocytized EIgG and GIgG, as assessed by electron microscopy, was complete at 24 and 3 h after injection, respectively. The depression of Kupffer cell complement receptor clearance function caused by EIgG and GIgG returned to normal by 6 h after injection of EIgG and by 3 h after injection of GIgG. Phagocytosis of EIgG depressed the survival rate after endotoxemia and bacteremia when endotoxin or bacteria were injected at 30 min after EIgG. The survival rate returned to normal when the endotoxin and bacteria were injected at 12 and 6 h after the EIgG, respectively. Phagocytosis of GIgG did not depress the survival rate after endotoxemia and bacteremia. Thus, compared with erythrocytes, erythrocyte ghosts are more rapidly digested after phagocytosis, depress complement receptor function for a shorter period of time, and cause less depression of host defense. These findings indicate that the contents of erythrocytes play an important role in the impairment of host defense caused by the phagocytosis of erythrocytes by Kupffer cells.
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PMID:Effect of Kupffer cell phagocytosis of erythrocytes and erythrocyte ghosts on susceptibility to endotoxemia and bacteremia. 362 92

Previous work has demonstrated that in vivo hepatic macrophage complement receptor clearance function is depressed following thermal injury. The present study was carried out to determine if complement receptor function depression is associated with other states of depressed host defense. Hepatic complement receptor clearance function was determined from the hepatic uptake of rat erythrocytes coated with antierythrocyte IgM (EIgM) in rats. Receptor function was determined following cannulation of a carotid artery, laparotomy plus enterotomy, hemorrhagic shock, trauma, thermal injury, acute bacteremia, acute endotoxemia, and injection of erythrocyte stroma, gelatinized lipid emulsion, or colloidal carbon. Hepatic uptake of EIgM was depressed following each of these experimental interventions except arterial cannulation. This effect was shown not to be due to a decrease in hepatic blood flow or depletion of complement and was therefore due to a depression in hepatic macrophage complement receptor clearance function. Thus, impairment of hepatic macrophage complement receptor function is associated with several states of depressed host defense.
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PMID:Hepatic macrophage complement receptor clearance function following injury. 395 Dec 17

Organ interactions are increasingly recognized as key determinants of the pathogenesis and potential for resolution of tissue injury during critical illness. A paradigm for a systems model that takes into account the modulatory effects of organ interactions and incorporates the expanding number of molecular and cellular pro-inflammatory networks is still lacking. Unifying hypotheses for multiple organ dysfunction during the systemic inflammatory response syndrome have been slow to emerge. The liver plays a central role in the regulation of multiple host defense, immunologic, biochemical, and metabolic functions during sepsis and trauma. However, the liver is relatively inaccessible for clinical study and its function is often non-specifically defined. Consequently, the liver's pathogenetic importance within a regulatory network of mediator and organ interactions during inflammatory responses leading to acute lung injury is poorly appreciated. This review addresses the concept that hepatic performance, broadly defined, represents a point of convergence in which four regulatory elements of the acute inflammatory response interact over a host defense continuum to affect lung function. These regulatory elements include: a) control of systemic endotoxemia, bacteremia, and vasoactive by-products of sepsis and trauma by the gut-liver axis of inflammation, mononuclear phagocytic clearance, and Fc and complement receptor-mediated events; b) production and export of endogenous cytokine and eicosanoid mediators by Kupffer cells, especially in relation to changes in the prevailing hepatic oxygen supply; c) metabolic inactivation and detoxification of such mediators via cell-to-cell interactions at the Kupffer cell-hepatocyte interface; and d) cytokine-driven synthesis of acute-phase proteins that critically modulate metabolism and inflammation. Our goal is to summarize and integrate recent information that sheds light on mechanisms by which hepatic function modulates host defense homeostasis, thereby influencing pulmonary function in the adult respiratory distress syndrome. Liver-lung interactions are presented as a heuristic paradigm of organ interactions that dynamically modulate systemic immunophysiologic responses during critical illness.
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PMID:Liver-lung interactions in critical illness. 780 98