Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous data from our laboratory have demonstrated that glucan administration significantly alters the course of a variety of experimentally induced infectious diseases. In view of the increasing incidence of gram-negative infections, studies were initiated to evaluate the effect of intraperitoneal glucan therapy on Escherichia coli-induced peritonitis and sepsis. Male ICR/Tex mice were injected intraperitoneally with glucan or dextrose on days 5 and 3 prior to intraperitoneal challenge with 1.0 x 10(8) E. coli. Glucan administration resulted in a significant enhancement of survival. Evaluation of the mechanism of protective action of glucan revealed that both the glucan and dextrose control groups showed an equivalent level of blood-borne E. coli at early periods. At 6 hours after challenge the glucan group showed a significant decrease in blood-borne E. coli. In contrast, the dextrose control group demonstrated progressive bacteremia. A significant depression of phagocytic activity occurred in E. coli-infected mice as compared with control mice that were not exposed to the bacterial challenge. The enhancement in phagocytic function observed in glucan-treated control mice was unaltered in E. coli challenged, glucan-treated mice. The possible importance of hyperfunctional macrophages in reduction of mortality from E. coli sepsis was denoted by methyl palmitate-induced reversal of the glucan hyperfunctional state. Methyl palmitate-treated glucan injected mice were not protected against E. coli infection. These data denote that the intraperitoneal administration of glucan significantly modifies the course of E. coli-induced peritonitis and bacteremia due, in part, to glucan-induced enhancement of macrophage function.
 ...
PMID:Immunotherapeutic modification of Escherichia coli--induced experimental peritonitis and bacteremia by glucan. 633 16

The enhanced risk of severe sepsis following splenectomy is now well recognized in both adult and pediatric patients. Prophylactic antibiotics and bacterial vaccines have been utilized with limited success to inhibit the high morbidity and mortality. This study reports the use of glucan, a beta-1,3-polyglucose, as a nonspecific immunostimulant for postsplenectomy pneumococcal sepsis. ICR mice were treated with glucan or glucose (5% w/v) following splenectomy or sham operation. Mice were then challenged with 1 X 10(9) Streptococcus pneumoniae intranasally. Glucan significantly increased survival in the splenectomy group (75%) compared to controls (27%). Phagocytic function, as measured by the clearance of 131I-triolein-labeled reticuloendothelial test lipid emulsion, was increased in the glucan group when compared to control glucose animals, both in the presence and absence of pneumococcal infection. Splenectomy alone did not significantly decrease phagocytic function. An increased leukocytosis in response to pneumococcal infection was observed in splenectomized glucan-treated animals. Nonspecific immunostimulation appears to have significant potential as a treatment strategy against postsplenectomy infection.
 ...
PMID:Protective effect of nonspecific immunostimulation in postsplenectomy sepsis. 665 37

Glucan, a beta-1,3 polyglucose, was evaluated for its ability to enhance resistance of post-operative mice to experimentally induced C. albicans sepsis. Male C57BL/6J mice were injected i.v. with glucan (0.45 mg/mouse) on days 10,7,4 and 1 prior to midline laparotomy and intravenous challenge with 3 X 10(6) C. albicans. The detrimental effect of surgery on survival following C. albicans infection was manifested by a 47% survival in the non-surgery-infected group in contrast to 20% in the surgery-infected group. Protection against C. albicans was observed in the glucan-treated groups. The glucan-treated non-operated mice manifested 100% survival while the surgery group had a 73% survival. Glucan significantly enhanced macrophage phagocytic function in control and operated mice. Laparotomy alone did not significantly depress macrophage phagocytosis. Histopathological studies revealed that glucan markedly inhibited the renal pathology associated with C. albicans challenge both in the presence and absence of laparotomy. These data indicate that glucan increased survival and reduced renal pathology associated with C. albicans challenge in the post-operative period. These observations suggest that Biologic Response Modifiers such as glucan may be effectively employed in patients who are at risk for post-operative infections.
 ...
PMID:Modification of post-operative C. albicans sepsis by glucan immunostimulation. 672 65

Glucan, a beta-1-3-polyglucosidic component of the cell wall of Saccharomyces cervisiae, was evaluated for its ability to influence the survival rate in rats with induced intraabdominal sepsis. To mimic closely the human bacteriological intestinal flora, the rats, in 4 groups each of 15 animals, were fed a lean meat diet. Intraabdominal sepsis was induced by resecting 1 cm of the intestine and reimplanting it in the abdominal cavity, reestablishing intestinal continuity by one-layer end-to-end anastomosis. The rats were injected with glucan, isovolumetric saline, and ampicillin or glucan plus ampicillin. The results indicate a significant decrease in mortality in the group treated with ampicillin compared with the group treated with saline only. The group treated with glucan plus ampicillin differed significantly from the group given ampicillin. The bacterial flora was not qualitatively influenced by glucan administration. It is concluded that glucan, in combination with ampicillin, has a significant effect on the survival rate of rats with induced peritonitis, probably by enhancing the activities of the reticuloendothelial system--an important part of the total host resistance.
 ...
PMID:The effect of glucan--a host resistance activator--and ampicillin on experimental intraabdominal sepsis. 716 67

Glucan, a 1-3-polyglucosidic component of the cell wall of Saccharomyces cerevisiae, was evaluated for its ability to alter survival in rats with induced intraabdominal sepsis. In four groups, each of 15 rats, the bacteriological flora was changed into that of humans by giving the animals a meat chew. Intraabdominal sepsis was induced by resecting 1 cm of the intestine and reimplanting it in the abdominal cavity after reestablishing the intestinal continuity by one-layer end-to-end anastomosis. The rats were injected with either glucan or isovolumetric saline or benzylpenicillin or glucan plus benzylpenicillin. The results indicate no significant difference in mortality rate between the groups treated with either glucan or benzylpenicillin on the one hand and, on the other, the group given saline alone. However, the group treated with glucan plus benzylpenicillin differed significantly from the control group given just saline. The bacterial flora did not seem to be influenced by glucan administration. It is concluded that glucan has a clear effect on the survival rate of rats with induced peritonitis, probably by enhancing the activities of the reticuloendothelial system--an important part of the total host resistance.
 ...
PMID:Glucan-induced enhancement of host resistance in experimental intraabdominal sepsis. 717 85

In a effect to prevent nosocomial pneumonia and sepsis, we treated patients with severe multiple trauma with an immunomodulator--beta 1-3 polyglucose (glucan). Forty-one patients with no infection at admission were stratified using Trauma Score and included in a randomized double-blind controlled trial. They were divided into a control group (n = 20) and a glucan group (n = 21). Pneumonia occurred in 11 of 20 patients in the control group and in two of 21 recipients of glucan (p < 0.01). Sepsis occurred in seven of 20 patients in the control group and in two of 21 patients treated with glucan (p < 0.05). Considering patients with pneumonia and sepsis, a decrease was observed in nosocomial infection from 65.0 to 14.4 percent (p < 0.001). The mortality rate related to infection was 30.0 percent in patients in the control group and 4.8 percent in the group treated with glucan (p < 0.05). The general mortality rate, cerebral deaths excluded, was 42.1 percent in the control group and 23.5 percent in the glucan group.
 ...
PMID:Infection prevention in patients with severe multiple trauma with the immunomodulator beta 1-3 polyglucose (glucan). 821 83

Interleukin-1 (IL-1), a cytokine released from macrophages by endotoxin stimulation, has been shown to upregulate the genetic expression of the hepatocyte growth factor (HGF). The present study was conducted to determine whether plasma HGF is increased in patients with systemic inflammatory response syndrome (SIRS). The plasma levels of HGF, endotoxin, and beta-glucan were measured in 41 surgical patients without hepatic diseases, 18 of whom had been diagnosed with sepsis, and 33, with nonseptic SIRS. The plasma HGF was found to be significantly increased in the 18 patients with sepsis, at 0.69 +/- 0.47 ng/ml (mean +/- SD), and in the 23 patients with nonseptic SIRS, at 0.49 +/- 0.37 ng/ml, compared to values in 40 normal controls, at 0.10 +/- 0.03 ng/ml (P < 0.001). No significant correlations were observed between the plasma levels of HGF and endotoxin (r = 0.02) or beta-glucan (r = -0.05) in any of the patients; however, plasma HGF was significantly correlated with the WBC count (r = 0.34, P < 0.05) and with total bilirubin (r = 0.45, P < 0.01). Plasma HGF was also strongly correlated with alanine transaminase (ALT) in 8 patients with ALT levels higher than 50 U/l (r = 0.70), but there was no such correlation in 33 patients with ALT levels of 50 U/l or less (r = 0.30). Thus, although the clinicopathologic significance of HGF is not well understood, the present findings indicate that plasma HGF increases in response to infection or inflammation.
 ...
PMID:Plasma hepatocyte growth factor levels are increased in systemic inflammatory response syndrome. 872 43

Plasma endotoxin contents of the patients with sepsis or typhoid fever were measured by two sophisticated chromogenic limulus tests; Endospecy and Toxicolor tests. Endospecy test is the endotoxin-specific test and Toxicolor is responsible for both endotoxin and (1,3)-beta-D-glucan. Plasma was pretreated by our new PCA method which resolved the problem as to the detection of a lesser amount of plasma endotoxin when pretreated by the conventional PCA method. Although Toxicolor values have been reported to exceed more than the Endospecy value, under complicated pathophysiological situations, almost all specimens of these patients had a similar value, except in one expired septic shock case. In 18 typhoid fever cases, Salmonella typhi was isolated only from the bile in 5 cases, however endotoxemia occurred in 11 cases (61.1%). Within the first 4 days, the incidence of endotoxemia was higher (10/14, 71.4%). These results suggest that endotoxin assay seemed to be a useful tool for the diagnosis of typhoid fever.
 ...
PMID:Plasma endotoxin in typhoid fever. 892 38

The emergence of multiple antibiotic-resistant microorganisms has led to a search for alternatives to traditional therapeutic regimens. PGG glucan is a soluble beta-glucan immunomodulator that selectively enhances the microbicidal activities of neutrophils and macrophages without stimulating proinflammatory cytokine production. In the present studies, we examined the ability of PGG glucan to act in concert with antibiotics to decrease mortality in a rat model of intraabdominal sepsis using antibiotic-resistant bacteria as infectious inocula. Results of these studies demonstrated that prophylaxis with PGG glucan in combination with antibiotics provided enhanced protection against lethal challenge with Esherichia coli or Staphylococcus aureus as compared with the use of antibiotics alone.
 ...
PMID:Prophylaxis with the immunomodulator PGG glucan enhances antibiotic efficacy in rats infected with antibiotic-resistant bacteria. 899 82

Although glycosylphosphatidyl-inositol (GPI) linked membrane proteins do not possess transmembrane or cytosolic sequences they elicit transmembrane signals. Using microscopic fluorescence imaging and resonance energy transfer (RET) techniques we have shown that certain pro-inflammatory GPI-linked membrane proteins can interact with leukocyte beta 2 integrins (complement receptor type 3 (CR3) and 4 (CR4) and the leukocyte function-associated antigen-1 (LFA-1)). For example, physical associations between CR3 and Fc gamma RIIIB, CR3 and urokinase receptors, and CR3 and CD14 (lipopolysaccharide receptor) have been found. Although Fc gamma RIIIB appears to be constitutively associated with CR3, urokinase receptors and CD14 associations with CR3 are influenced by their ligation status and cell function (e.g. adherence and locomotion). CR3-to-urokinase receptor interactions have been confirmed by immunoprecipitation techniques. Immunoprecipitation of CR3 from Brij-58 lysates after biotinylation of neutrophil membranes revealed proteins of M(r) = 40,000, 50,000, 74,000 and 120,000, in addition to bands corresponding to the integrin alpha and beta chains. Cell functions such as transmembrane signaling and superoxide release/priming have been linked to these interactions. Importantly, reagents that affect the lectin-like site of CR3, such as N-acetyl-D-glucosamine, alpha-methyl-D-mannoside and beta-glucan alter these interactions and, in parallel, leukocyte functions. Thus, the interactions of GPI-linked proteins and integrins can be highly dynamic events linked to cell activities. Our studies suggest that it may be possible to develop new drugs directed at the lectin-like site of beta 2 integrins that block GPI-linked protein-to-integrin coupling thereby controlling inflammatory cell processes including cell adherence, locomotion and activation. Such drugs may be useful in clinical conditions such as ischemia-reperfusion injury, sepsis, arthritis and others.
 ...
PMID:Ectodomain interactions of leukocyte integrins and pro-inflammatory GPI-linked membrane proteins. 922 70


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>