Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endolymphatic infusions of an antibacterial complex (antibiotic--lysozyme--proteinase inhibitor) resulted in recovery of 92,6% of patients after a complex treatment of diffuse peritonitis and sepsis. Gauze-sorbent tampons used in empyema of pleura give rapid cleaning of the cavity walls from pyo-necrotic masses and decreased the activity of the inflammatory process.
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PMID:[Administration of medications via a lymphatic vessel in the treatment of diffuse peritonitis and sepsis]. 399 8

The appearance of the adult respiratory distress syndrome (ARDS) during the course of acute illness is believed to result, in part, from intrapulmonary neutrophil sequestration and degranulation induced by circulating inflammatory mediators. To evaluate the role of complement-neutrophil interactions in the pathogenesis of ARDS in man, 34 patients suffering from intra-abdominal sepsis (seven), multisystem trauma (15), or acute pancreatitis (12) were serially studied with regard to neutrophil migratory responses to C5a and F-Met-Leu-Phe, lysosomal content of beta-glucuronidase and lysozyme, and simultaneously obtained plasma levels of immunoreactive C3adesArg and C5adesArg. Nineteen patients developed ARDS. In these patients, plasma C3adesArg levels obtained within 72 hours of admission to the hospital were elevated to 305 +/- 35 ng/ml compared with 145 +/- 16 ng/ml for patients who did not develop ARDS (p less than 0.0005). C5adesArg levels were not elevated in either group. In vitro studies showed that neutrophils from normal persons were able to clear all of the C5a/C5adesArg generated in up to 5% zymosan-activated serum, while no clearance of C3adesArg was identified. Patient migratory responses could be divided into three groups based on their initial (less than 72 hour) samples: (1) hyperresponsive to both N = formyl-methionyl-leucyl-phenylalanine (FMLP) and C5a, (2) specifically deactivated to C5a, and (3) deactivated to both C5a and FMLP. Patients in the latter two groups developed ARDS. Enzyme content of neutrophils from patients who developed ARDS showed a substantial fall in beta-glucuronidase and lysozyme levels. The finding of elevated plasma C3a levels and deactivation of migratory response to C5a support the contention that complement activation had occurred in these patients and that their neutrophils had been exposed to C5a/C5adesArg in vivo. The finding of nonspecific migratory dysfunction associated with lysozymal enzyme loss, a circumstance not reproducible in vitro by C5a exposure, suggests that other stimuli produced degranulation of neutrophils made hyperresponsive by prior exposure to C5a.
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PMID:Complement activation and clearance in acute illness and injury: evidence for C5a as a cell-directed mediator of the adult respiratory distress syndrome in man. 400 15

Prominent and global abnormalities in chemotactic, oxidative, and microbicidal activity have been identified in neutrophils from patients with severe sepsis. To evaluate the possible contribution of degranulation as the basis for the observed abnormalities, 12 patients with intrabdominal infection were serially studied and neutrophil chemotaxis, enzyme content, and receptors for FMLP were evaluated. There was a significant correlation between chemotactic response to both activated serum and FMLP with the granular enzymes beta-glucuronidase and lysozyme. For FMLP-directed migration, r = 0.73, P less than 0.001 for lysozyme, and r = 0.59, P less than 0.001 for beta-glucuronidase. There was a similarly significant correlation between loss of lysozyme and an increase in FMLP receptors, previously shown to be a marker for degranulation. These data support the concept that in vivo degranulation, possibly due to effects of circulating chemoattractants on adherent neutrophils, is responsible for the enzymatic and chemotactic loss seen in cells from septic patients. This hypothesis also provides a mechanism to explain the respiratory distress syndrome if degranulation were to occur in the pulmonary capillary bed.
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PMID:Neutrophil dysfunction in sepsis. III. Degranulation as a mechanism for nonspecific deactivation. 632 15

The effects of season and variations in the prevalence of infectious disease on the concentrations and daily production of breast-milk immunoproteins were studied in 152 rural Gambian mothers and their children up to 26 months post-partum. IgA, IgG, IgM, C3, C4, lactoferrin, lysozyme and secretory component concentrations and breast-milk volumes were measured longitudinally over a six month period which encompassed dry and rainy seasons. No increase in the production of any immunoprotein was observed at the time of maximum prevalence of serious infectious diseases, especially diarrhoea, in the children. Enhanced secretion of certain immunoproteins was noted in mothers of children aged 9-18 months at the beginning of the rainy season. There was some evidence that this may have been associated with skin sepsis, particularly impetigo, in the children. The production of most immunoproteins fell during the rainy season. This was not the result of declining maternal food intakes as similar decreases were seen for women receiving a dietary supplement.
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PMID:Breast-milk antimicrobial factors of rural Gambian mothers. II. Influence of season and prevalence of infection. 654 89

Lysozyme levels were determined in serum and umbilical cord blood of 352 newborns and prematures. Levels in premature babies were found to be significantly lower than those of matures at the first day of life. A correlation was seen between the serum lysozyme and the birth weight of 219 mature newborns. In 14 premature babies with clinical signs of sepsis the concentrations of serum lysozyme were particularly decreased in cases of septicemia caused by gram-negative organisms. Serum levels of lysozyme in cord blood were significantly lower in 38 newborns with predisposition to septicemia (above all premature rupture of membranes greater than 24 hr.) comparing with healthy infants. The decreased serum levels of lysozyme in newborns with septicemia and the remarkable susceptibility of infections in male newborns are discussed.
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PMID:[Serum lysozyme activity of serum and umbilical cord blood in newborn babies-diagnostic value of the enzyme in infants with susceptibility to infections and in cases of septicemia. (author's transl)]. 719 43

Serum levels of lysozyme were studied in 43 term and 36 premature newborns. Levels in premature babies were found to be significantly (p less than 0,001) lower than those of matures. Observation over two weeks revealed a rise of serum lysozyme in premature babies and a decline in mature newborns. The level seems to depend upon the turnover of neutrophile granulocytes. In 5 premature babies with clinical signs of sepsis the serum lysozyme concentrations were significantly (p less than 0,01) lower than those in healthy prematures. It is assumed that the activity of the intraneutrophilic lysozyme in patients with bacterial infections is reduced to as little as 50%. Urine controls for lysozyme in 43 newborns (mature and premature) did not show evidence of measurable lysozyme concentrations.
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PMID:[Serum lysozyme activity in term and preterm newborns (author's transl)]. 736 Jan 22

Bacterial lipopolysaccharide (LPS) stimulates the production and release of endogenous mediators [e.g., tumor necrosis factor (TNF), interleukins-1 and -6 (IL-1 and IL-6), and Platelet Activating Factor [PAF] responsible for the pathophysiologic changes and the mortality associated with sepsis. We recently demonstrated that lysozyme (LZM) bound to LPS (LZM-LPS complex) suppresses LPS-induced tumor necrosis factor-alpha (TNF-alpha) production in vivo. In the present study, we investigated the effect of LZM-LPS complex formation on LPS-induced IL-6 production, both in vitro and in vivo. With the addition of LZM-LPS complex, TNF-alpha and IL-6 release was significantly reduced compared with that by LPS in a dose-dependent manner in mouse macrophage-like cells, RAW264.7. IL-6 production in serum by LPS in carrageenan (CAR)-primed mice peaked at 2 hr following injection. LZM-LPS and LZM-Escherichia coli cell complex (as 1 microgram of LPS per mouse) released significantly reduced concentrations of IL-6 in serum (P < 0.01 and P < 0.001 versus CAR-pretreated LPS- or cell-injected mice). These results emphasize the important role of LZM in vivo in the neutralization of endotoxin. However, in the case of IL-6, by administration of a lethal dose of LPS (as 100 micrograms of LPS per mouse), the IL-6 level was reduced by LZM, but a significant concentration of IL-6 was still released; although the TNF- alpha concentration was negligible in this experimental condition. Thus, it is suggested that LZM might regulate the systemic inflammation induced during Gram-negative bacterial infections by inhibiting the release of cytokines in serum.
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PMID:Lysozyme regulates LPS-induced interleukin-6 release in mice. 762 57

Although prolonged Gram-negative sepsis with high permeability alveolar edema, a well documented cause of adult respiratory distress syndrome, has been shown to result in surfactant alterations, the effects of acute endotoxemia on the lung surfactant system are largely unknown. In this study, lethal endotoxemia (> 80% mortality at 24 h) resulting in severe, rapid leukopenia with progressive thrombocytopenia was achieved through intraperitoneal injection of adult Fischer 344 rats with 3.5 mg of Escherichia coli endotoxin/kg. After assessment of pulmonary mechanics under general anesthesia, endotoxin-injected rats and appropriate controls were killed at 4, 8, and 12 h for morphological and biochemical analyses. Morphometric estimation of surfactant membrane subtypes in bronchoalveolar lavage fluid revealed prominent alterations including significant decrease (45%) in tubular myelin 12 h post-endotoxin, with a threefold increase in lamellar body-like forms at 8 and 12 h. Acute endotoxicosis resulted in decrease of total dynamic compliance, whereas pulmonary resistance remained unchanged. These changes were associated with margination of polymorphonuclear leukocytes in lung microcirculation, multifocal septal edema, and decrease in lamellar body lysozyme specific activity at 12 h. Alveolar edema, as determined by measurement of total protein in cell-free bronchoalveolar lavage fluid, was absent in both controls and endotoxin-injected rats. The results indicate that bloodborne lung injury induced by lethal endotoxicosis initiates acute perturbation of secreted surfactant membranes with pulmonary dysfunction in the absence of high protein alveolar edema.
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PMID:Depletion of surfactant tubular myelin with pulmonary dysfunction in a rat model for acute endotoxemia. 774 73

Examinations of 230 patients with local pyogenic infection and those of 117 patients with sepsis revealed that asporogenic anaerobes on pure culture were isolated in 17.8% with local pyosis and in 10.2% of patients with sepsis. Anaerobes along with aerobic microbes were found 15.6% of patients with local infection and in 10.2% of patients with sepsis. The involvement of obligate anaerobes in the development of pyogenic infection was displayed by the lower phagocytic activity of neutrophils, the impaired differentiation of lymphocytes, the great increased peripheral blood levels of O-cells, and diminished serum complementary, lysozyme, and overall bactericidal activities and IgM levels.
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PMID:[Microbiology and immunology of suppurative surgical infection caused by non spore-forming anaerobes]. 865 52

Phagocytic cells, such as polymorphonuclear neutrophils, monocytes, and macrophages, are essential for defense against infection caused by a variety of microorganisms. The mechanisms used by these cells to destroy microbes comprise a potent oxidative armamentarium including superoxide, hydrogen peroxide, and hypochlorous acid. In addition, granule contents such as proteolytic enzymes, lysozyme, lactoferrin, and myeloperoxidase are released into the phagosome to destroy ingested microorganisms. Inflammatory cytokines, such as tumor necrosis factor (TNF), interleukin-1 (IL-1), and IL-6, enhance the phagocytic and microbicidal activity of the cells and increase their stickiness. It has been demonstrated in a variety of animal and clinical studies that activated phagocytes can damage the host they are designed to protect, using the mechanisms described above. Alkylxanthines, including pentoxifylline, are potent inhibitors of this inflammatory damage by two major actions: (a) reduction of the production of inflammatory cytokines (especially TNF) by phagocytes stimulated with a variety of microbial products (e.g., endotoxin); and (b) reversal of the effect of these cytokines on phagocytes. Thus, pentoxifylline counteracts the following effects of inflammatory cytokines on phagocytes: increased adherence, shape change resulting in larger size and rigidity, increased oxidative burst, priming for an enhanced oxidative burst, increased degranulation, and decreased chemotactic movement. In addition, these activities synergize with the normal anti-inflammatory mediator adenosine. Alkylxanthines have the potential to be effective therapy for conditions in which inflammatory cytokines and phagocytes cause damage, including the sepsis syndrome, ARDS, AIDS, and arthritis.
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PMID:Cytokines, phagocytes, and pentoxifylline. 869 56


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