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

Activated polymorphonuclear leukocytes (PMNs) are implicated in the pathogenesis of acute lung injury (ALI) associated with sepsis. Adhesion of activated PMNs to endothelial monolayers is mediated by the CD18 adhesion-receptor complex on the PMN cell surface. Monoclonal antibody 60.3 (MoAb 60.3) blocks CD18-dependent PMN-endothelial adhesion in vitro and in vivo. This study was designed to determine the role of CD18-dependent PMN adhesion in ALI associated with gram-negative sepsis. Anesthetized, ventilated (FiO2 0.5, positive end-expiratory pressure 5 cm H2O) pigs received sterile saline (control, n = 8) or live Pseudomonas aeruginosa, 5 x 10(8) colony-forming units/ml at 0.3 ml/20 kg/min (septic, n = 9) for 1 hour. A third group (n = 7) received MoAb 60.3, 2 mg/kg intravenously, 15 minutes before Pseudomonas infusion. Animals were studied for 300 minutes. MoAb 60.3 significantly (p less than 0.05) attenuated the neutropenia seen in sepsis (15 +/- 1 vs 6 +/- 1 x 10(3) PMNs/mm3 at 300 min). Alveolar-capillary membrane injury was assessed by bronchoalveolar-lavage protein content and extravascular lung water determination. MoAb 60.3 significantly (p less than 0.05) reduced BAL protein at 300 minutes (388 +/- 75 vs 1059 +/- 216 micrograms/ml in septic animals) and attenuated the increase in extravascular lung water to 240 minutes (7.1 +/- 2 vs 14.2 +/- 1.2 ml/kg in septic animals). Systemic hypotension, decreased cardiac index, pulmonary hypertension, and relative hypoxemia, all characteristic of this model, were not altered by MoAb 60.3. These data suggest that, in this model of septic ALI, neutropenia is, in part, CD18 dependent and that blocking CD18-dependent PMN adhesion protects the alveolar-capillary membrane independently of altered hemodynamic status.
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PMID:Anti-CD18 antibody attenuates neutropenia and alveolar capillary-membrane injury during gram-negative sepsis. 167 91

A method was developed to study the adhesion of Streptococcus pneumoniae to human pharyngeal epithelial cells. Epithelial cells from healthy persons, pneumococcal strains from patients with otitis media, meningitis, or septicemia, and pneumococcal cells from the nasopharynx of healthy carriers were used. Adhesion was found to be influenced by changes in the bacterial incubation medium and growth phase, the concentration of bacteria and epithelial cells, the epithelial cell donor, the incubation time and temperature, and the pH and osmolarity of the incubation medium. Pretreatment of bacteria with heat, Formalin, or trypsin decreased adhesion. The highest adhesion was obtained when 10(9) bacteria cultivated for 18 h in streptococcus cultivation broth were added to 10(4) pharyngeal cells and incubated at 37 degrees C for 30 min. S. pneumoniae strains from patients with frequent episodes of otitis media and strains from healthy carriers had the highest adhesion values; septicemia and meningitis strains had the lowest. The capsular polysaccharide type did not determine the adhesive capacity of the strains, but otitis strains belonging to the capsular types often associated with otitis media adhered in high numbers. Adhesion may be important for pneumococci colonizing the nasopharynx or inducing otitis media.
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PMID:Adhesion of Streptococcus pneumoniae to human pharyngeal epithelial cells in vitro: differences in adhesive capacity among strains isolated from subjects with otitis media, septicemia, or meningitis or from healthy carriers. 721 90

Adhesion molecules play a critical role in the interaction of circulating neutrophils with vascular endothelium during inflammation. Increased quantities of soluble, circulating intercellular adhesion molecule-1 (cICAM-1) are present in various inflammatory conditions. The purpose of this investigation was to measure cICAM-1 levels in septic adults, as well as to examine the relationship between this potential marker of endothelial-cell activation and the consequences of sepsis (i.e., multiple organ failure and death). Using a sandwich-type enzyme-linked immunosorbent assay (ELISA), we measured cICAM-1 in blood samples obtained within 12 h of admission to an intensive care unit (ICU) for sepsis and other conditions. We found cICAM-1 levels to be increased in 25 septic patients (1,259 +/- 159 ng/ml, mean +/- SEM) as compared with 12 healthy volunteers (355 +/- 41 ng/ml, p < 0.0001) and four ICU patients without systemic inflammatory response syndrome (SIRS) (585 +/- 76 ng/ml, p < 0.001). Twenty-five patients with SIRS but no evidence of causative infection also had elevated levels of cICAM-1 (937 +/- 144 ng/ml, p = 0.12 versus sepsis). Serial measurements over the first week of sepsis demonstrated persistent elevation in most patients. Day 1 cICAM-1 levels were higher (p = 0.017, ANOVA) in 16 patients with septic shock than in seven with severe sepsis and two with sepsis but without hypotension or hypoperfusion. There was a positive correlation (r = 0.50, p = 0.009) between Day-1 cICAM-1 measurements and severity of shock as determined by the presence of hypotension and vasopressor use.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circulating ICAM-1 is increased in septic shock. 773 95

Adhesion of polymorphonuclear leukocytes (PMN) to endothelial cells is an early key event in the inflammatory response and plays an important part in the pathogenesis of septic shock, contributing to vascular and tissue injury. Lipopolysaccharides (LPS) activate endothelial cells to enhanced expression of adhesion molecules. We investigated the interaction of human PMN with resting and LPS-activated human umbilical vein endothelial cells. The activation of endothelial cells by LPS alone did not lead to direct functional or morphological changes as measured by detachment of the endothelial cells from a monolayer and transendothelial albumin flux. LPS induced an increased adhesion of unstimulated PMN to endothelial cells. This was accompanied by endothelial detachment and increased permeability across a monolayer. Endothelial cell lysis as measured by 51Cr release was unaffected. Stimulation of PMN with phorbol ester did not further increase adherence, detachment, or permeability. We conclude that LPS activates endothelial cells and renders cultured monolayers more susceptible to PMN-induced damage. This may provide further insight into the relationship between PMN activation and endothelial damage in Gram-negative sepsis.
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PMID:Lipopolysaccharide induces hyperadhesion of endothelial cells for neutrophils leading to damage. 775 24

Expression of S-fimbriae is frequent in Escherichia coli strains causing sepsis and meningitis in the newborn period. We analysed the ability of human skim milk to inhibit adhesion of S-fimbriated E. coli to human buccal epithelia. Adhesion was inhibited by up to 90% using colostrum (5%) and up to 50% with mature milk (5%), indicating that this anti-infective mechanism depends on the period of lactation. Elimination of up to 99% of immunoglobulins and 91% of lactoferrin by affinity chromatography had no effect on the inhibition of adhesion. After separation of high- (> 10 kD) and low-molecular-weight fractions of skim milk, only the fraction > 10 kD was found to be able to inhibit bacterial adhesion. In order to further characterize receptor molecules for bacteria, we investigated binding of isolated S-fimbriae to glycoprotein bands on Western blot strips. Fimbriae mainly bound to a high-molecular-weight band (> 200 kD). According to molecular weight and staining behaviour, this band most likely represents mucins. We conclude that carbohydrate residues on secreted mucins of human skim milk are able to inhibit bacterial adhesion to mucosal surfaces. This could provide protection against neonatal sepsis and meningitis caused by E. coli.
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PMID:Inhibition of adhesion of S-fimbriated E. coli to buccal epithelial cells by human skim milk is predominantly mediated by mucins and depends on the period of lactation. 809 30

A 35-year-old male with sick sinus syndrome was complicated with recurrent local infection at the site of the generator pocket associate with a retained pacemaker lead, followed by septicemia presenting with Staphylococcus aureus. Several attempts to remove the lead via the implantation vein by direct traction were performed unsuccessfully because the leads were strongly adhered to the trabecula of the right ventricle. Repeated debridement employing antibiotic therapy was ineffective. As a last resort, we finally operated under extracorporeal circulation (ECC) 24 months after the first implantation and 22 months after initiation of the local infectious episode. As we found it difficult to remove the leads by traction even under direct vision, we used the vinyl chloride tube, which is a part of the ECC circuit, as a sheath for applying countertraction around the lead tip to prevent the myocardial wall from being torn and extracted together with the lead tip. The lead was removed successfully and a new epicardial lead was implanted. The postoperative course uneventful and no recurrence has occurred after 1 year. In reviewing the Japanese literature, 10 case, operated on under ECC to remove the infected retained leads, were described in detail. Among them, eight cases had undergone previous debridement including removal of the generator and the subcutaneous portion of the lead. It is clear that removal of all of the pacemaker system is necessary for eradication of infection. Adhesion of the lead to the wall is firm. Only one case besides ours succeeded in having its lead removed without requiring incision of the tissue around the lead tip.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Removal of infected total pacemaker system under extracorporeal circulation--a case report and review of the Japanese literature]. 830 77

Contaminated defects of the abdominal wall continue to be a significant problem for patients and surgeons. The lack of sufficient tissue may require the insertion of a prosthetic material. Polypropylene (PP) mesh is still the most widely used material for this purpose, although the propensity to induce extensive visceral adhesions and erosion of the skin or intestine is a well-known drawback. Expanded polytetrafluoroethylene (PTFE) patch has better mechanical properties and has a low potential for infection. Therefore, we used expanded PTFE patch to repair contaminated abdominal wall defects in three patients. In one patient, the postoperative course was uneventful. In the other two patients, the patch had to be removed for ongoing wound sepsis and because the patch disintegrated. In an experimental study, contaminated abdominal wall defects created in Wistar rats were repaired with expanded PTFE patch (PTFE group, n = 21) or PP (PP group, n = 21). Wound infection occurred in 16 rats in the PTFE group and in 14 rats in the PP group. Two rats in each group died. Two rats in the PTFE group died as a result of peritonitis, one rat in the PP group died as a result of ileus and one as a result of peritonitis. Incisional hernia was found to be significantly more frequent in the PTFE group (n = 13) than in the PP group (n = 3). Fistula formation was only found in three rats in the PP group. Adhesion formation was more pronounced in rats in the PP group. It is concluded that the expanded PTFE is unsuitable for the reconstruction of contaminated abdominal wall defects and that PP mesh is more suitable, although this material has a high risk of complications.
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PMID:Expanded polytetrafluoroethylene patch versus polypropylene mesh for the repair of contaminated defects of the abdominal wall. 842 1

Adhesion molecules on polymorphonuclear leukocytes (PMNL) play an important role in nonspecific defense mechanisms directed at invading microorganisms. When local infection, however, cannot be controlled, a systemic inflammatory response syndrome (SIRS) ensues which may progress to septic shock and multiple organ failure, these being major determinants of the patient's outcome. In the present study, the expression of beta 2-integrins and L-selectin on blood PMNL was measured on subsequent days in patients with sepsis (n = 17) and in healthy volunteers (n = 15). beta 2-Integrins and L-selectin molecules were detected by flow cytometry, using the monoclonal antibodies IB4 (anti-CD18) and Dreg200 (anti-CD62L), respectively. Adhesion molecules were determined at baseline immediately after blood collection and also 45 min after incubation of cells in vitro at body temperature to allow for spontaneous regulation. In addition, PMNL were activated by receptor-dependent and receptor-independent stimuli to characterize stimulus-specific adhesion molecule expression. In parallel with the measurement of adhesion molecules, severity of sepsis was assessed by the Elebute score. The results demonstrate significant differences in the basal, spontaneous and stimulus-induced expression of adhesion molecules between healthy volunteers, survivors (n = 11) and nonsurvivors (n = 6). Moreover, when survivors and nonsurvivors with severe sepsis (Elebute score > 12) were compared, basal expressions of both beta 2-integrins and L-selectin were significantly lower in patients who did not survive. Thus, measurement of adhesion molecules on circulating PMNL may be useful to identify septic patients at high risk for lethal outcome.
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PMID:Expression of beta 2-integrins and L-selectin on polymorphonuclear leukocytes in septic patients. 916 33

Bacteria have been associated with a wide variety of syndromes in animals and humans. These include enteropathies, urinary infections, meningitis and septicemia. Among the distinct set of tactics to prevail within the host, is the ability of bacteria to adhere to cellular targets. Adhesion to the gut by enteric bacteria occurs via several types of adhesins. During the last 15 years, much information has become available on bacterial adhesins and mechanisms governing bacteria-host interactions. Due to their location on the cell surface, establishing a carbohydrate frontier, and their inherent variability, glycosphingolipids and glycoproteins provide a wide range of binding sites for bacteria, toxins and more generally lectins. Bacterial lectins are localized either on the tip or along fimbrial filaments or on nonfimbrial structures. We examine in this short review, a collection of pathogen lectins, through their different receptor specificities. For sialic acid-binding lectins, the conformation of terminal sialic acid is essential for adhesion, whereas for other bacterial lectins, complementary sugars may be arranged in specific linear and/or branched sequences. Finally, it appears that the composition and structure of cell carbohydrates could in part explain the bacterial tropism and susceptibility or resistance of the host to enteric diseases.
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PMID:Interactions between the enteric pathogen and the host. An assortment of bacterial lectins and a set of glycoconjugate receptors. 919 3

Almost all respiratory diseases except benign lung tumors and lung dysplasia entail acute lung injury. The many clinical conditions associated with acute lung injury include aspiration pneumonia, bacterial pneumonia, and sepsis. The fundamental cause of acute lung injury is pulmonary vascular hyperpermeability. Pulmonary vascular hyperpermeability can be attenuated by nitric oxide and cyclic GMP, and potentiated by oxygen radicals and elastase released from neutrophils. Adhesion molecule inhibition could become an effective therapy against acute lung injury, because the adhesion molecules are very important in the pathogenesis of this condition. Adhesion molecules could also be useful markers of disease activity in various lung diseases. Neutrophil elastase inhibitors may become important as therapeutic agents against acute exacerbations of idiopathic interstitial pneumonia, because this pathological condition is a type of acute lung injury. Similarly, N-acetyl cysteine could also become a useful therapeutic agent against idiopathic interstitial pneumonia, because it is a precursor of glutathione, which is the major antioxidant in the fluid lining of the bronchial epithelium.
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PMID:[Pathophysiology of acute lung injury]. 921 75


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