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)

Seventy-four cultures of Pasteurella multocida representing all four capsular types, A, B, D, and C, from various animal species and diseases were examined for the production of hyaluronidase by two procedures. In one, hyaluronidase production was determined by the depolymerization of streptococcal capsular hyaluronic acid, and in the other, production was determined by degradation of sodium hyaluronidate in a solid culture medium. Hyaluronidase production was only demonstrated in the 13 type B cultures that had been recovered from cases of hemorrhagic septicemia.
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PMID:Hyaluronidase production by type B Pasteurella multocida from cases of hemorrhagic septicemia. 676 66

Light microscopic, histochemical, immunohistochemical, and ultrastructural methods were used to examine myocardial epithelial masses in the hearts of ten cattle. The tissues consisted of paraffin-embedded or formalin-fixed samples from eight hearts that were being inspected in slaughter houses and from two hearts from calves that died of septicemia. The ages of the cattle ranged from 4 days to 12 years; the breeds were unspecified for all but one Hereford female and the two Holstein calves; and there were three males, four females, and three steers. The masses in these cases were compared with similar appearing lesions found in other animal species. The lesions in the bovine hearts were single to multiple, well circumscribed, found in the left ventricle wall, and composed of squamous to cuboidal epithelial cells that formed tubular, ductular, and acinar structures with lumens that were void or filled with amorphous protein globules. Electron microscopic examination revealed epithelial cells that had sparse apical microvilli, tight apical intercellular junctions, perinuclear bundles of filaments, and rare cilia. Almost half of the bovine epithelial masses (4/9) had occasional diastase-resistant periodic acid-Schiff-positive granules in their cytoplasm, and few had hyaluronidase-resistant alcian blue-positive granules (2/9) or colloidal iron-positive granules (1/9). All myocardial masses had abundant collagen surrounding the tubular and acinar structures, and 2/9 had elastin fibers as well. None of the myocardial masses had Churukian-Schenk or Fontana Masson's silver staining granules in epithelial cells. Immunohistochemically, all bovine myocardial tumors stained positively for cytokeratin (8/8), and occasional masses stained positively for vimentin (3/8) or carcinoembryonic antigen (3/8). None of the masses stained positively for desmin. The myocardial epithelial tumors most likely represent endodermal rests of tissue misplaced during organogenesis.
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PMID:Bovine myocardial epithelial inclusions. 768 Jan 78

Neonatal Group B streptococcus (GBS) sepsis and pneumonia result in lung injury and remain a major cause of morbidity and mortality in the newborn. Increased lung hyaluronan (HA) content is an important component of the lung's early response to damage in diseases such as adult respiratory distress syndrome (ARDS), infant respiratory distress syndrome (IRDS), and bleomycin-induced fibrosis. It is known, however, that GBS virulence factors include specific secretory enzymes such as hyaluronidase, an enzyme which breaks down HA. We therefore hypothesized that in lobar GBS pneumonia, lung HA would be decreased compared with normal values, and that in lobar pneumonia with atelectasis, lung HA would be further decreased because of increased substrate availability. The right lower lobes (RLL) and left lower lobes (LLL) of anesthetized piglets 16 +/- 2 d old were each selectively inoculated with 1 x 10(9) colony-forming units (CFU) GBS via an endobronchial catheter (n = 7). The LLL was subsequently collapsed by endobronchial occlusion following 10 min of 100% O2. Control animals (n = 6) was anesthetized, instrumented, and ventilated without exposure to GBS. At 4 h, lungs were removed and HA extracted and assayed using a competitive inhibition assay. HA extracted from areas of lobar pneumonia was significantly decreased (27 +/- 6.6 micrograms/g wet lung, p < 0.005) when compared with control values of control piglets (51 +/- 19.6 micrograms/g wet lung). Atelectasis plus lobar pneumonia further decreased lung HA to 10 +/- 13.3 micrograms/g wet lung, p < 0.0001. We conclude that lobar GBS decreases lung HA and that this process is augmented by collapsed lung regions, and speculate that this departure from the usual early lung response to injury contributes to GBS invasion of lung parenchyma.
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PMID:Lung hyaluronan decreases during group B streptococcal pneumonia in neonatal piglets. 863 Jun 3

Group A streptococci (S. pyogenes) possess a number of capsule and cell wall associated components and release many extracellular proteins (toxins and hydrolytic enzymes) that are known or thought to contribute to the virulence and pathogenicity of the microorganism. Groupe A streptococci cause a wide array of infections, the most frequent of which are acute pharyngitis and pyoderma with two severe sequelae (acute rheumatic fever and glomerulonephritis). Other manifestations are scarlet fever and various soft tissue infections as well as sepsis and the recently characterized streptococcal toxic shock syndrome. The somatic components of group A streptococci include cell wall M protein, capsular hyaluronic acid, lipoteichoic acid, peptidoglycan, fibronectin binding protein, C5a peptidase and receptors for various human plasma proteins particularly IgA and IgG. The extracellular products are numerous and consist of among others the hemolytic toxins streptolysins S and O, hyaluronidase, streptokinase and cysteinyl proteinase as well as the superantigens erythrogenic toxins A and C also known as pyrogenic exotoxins.
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PMID:[Cellular constituents and extracellular proteins involved in the pathogenic capacity of Streptococcus group A]. 873 28

It is impossible to imagine modern medicine today without indwelling devices of various kinds. The time that these implants or prostheses remain in the patient's body can vary from a few hours, e.g. intravenous catheter, to his entire life, e.g. hip prosthesis, heart valve. Besides the indisputable use and advantages of this type of medical intervention for the patient, e.g. saving his life or improving its quality, the associated complications should not be overlooked. One of the most frequent and significant complications of implant surgery is the manifestation of infection in the tissue around the implant. That infection occurs is not surprising since the indwelling devices predispose to bacterial and mycotic infection on the one hand and impede its eradication on the other. The consequences of infection for the patient may mean the loss of regained mobility and independence, hospitalization for sepsis, or even death. Microbes per se are not necessarily pathogenic, however, there are numerous virulence factors which affect the degree of pathogenicity of the microorganisms. These include, for example, various enzymes, (e.g. catalase, hyaluronidase, collagenase and other proteases), and specific surface structures, e.g. the polysaccharide capsules of pneumococci or the lipopolysaccharides of Gram negative bacteria, and the production of bacterial toxins, e.g. leucozidin, streptolysine. The strategies which the pathogenic bacteria employ in their efforts to occupy the host include adherence, penetration and multiplication, antiphagocytosis and serum resistance, the formation of siderophores, antiimmunity, and cell and tissue damage. An attempt will be made here to present an overview of this multifactorial event in which the host obviously plays an important role.
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PMID:Relevance, pathogenicity and virulence of microorganisms in implant related infections. 903 48

A study of the uncharacterized serum inhibitors of hyaluronidase, first described half a century ago, was undertaken. Activity was measured against bovine testicular hyaluronidase using a microtiter-based assay and reverse hyaluronan substrate gel zymography. The predominant inhibitory activity was magnesium-dependent and could be eliminated by protease or chondroitinase digestion and by heat treatment. Kinetics of inhibition were similar against hyaluronidases from testis and snake and bee venoms. The inhibitor had no effect on Streptomyces hyaluronidase, indicating that inhibition was not through protection of the hyaluronan substrate. Inhibition levels in serum were increased in mice following carbon tetrachloride or interleukin-1 injection, inducers of the acute-phase response. Reverse zymography identified a predominant band of 120-kDa relative molecular size, with two bands of greater and one of smaller size. The predominant protein was tentatively identified as a member of the inter-alpha-inhibitor family. Inhibition was also observed using either purified inter-alpha-inhibitor or an inter-alpha-inhibitor-related 120-kDa complex. Inter-alpha-inhibitor, found in the hyaluronan-rich cumulus mass surrounding mammalian ova and the coat of fibroblasts and mesothelial cells, may function to stabilize such matrices by protecting against hyaluronidase degradation. Turnover of circulating hyaluronan is extraordinarily rapid, with a half-life of 2-5 min. Prompt increases in levels of serum hyaluronan occur in patients with shock, septicemia, or massive burns, increases that can be attributed, in part, to suppression of degradation by these acute-phase reactants, the inhibitors of hyaluronidase.
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PMID:Evidence that the serum inhibitor of hyaluronidase may be a member of the inter-alpha-inhibitor family. 1090 71

Streptococcus constellatus, S. intermedius, and S. anginosus, the three species of the S. milleri group, form part of the normal flora most commonly found in the mouth, throat, gastrointenstinal tract, and genital tract. The S. milleri group has become known as an important pathogen in abscess disease, but little attention has been paid to their role in deep neck abscesses. We have treated 9 patients with deep neck abscesses relating to the S. milleri group since 1991, and regarded this group as an important pathogen also in these abscesses. We studied the frequency of the S. milleri group isolated from deep neck abscesses in our cases and from the literature and discuss clinical significance and bacteriological pathogenesis. Cases numbered 27 treated at our facility since 1991 and 200 cases reported in the Japanese literature since 1990. Of our 9 cases, 4 originated from acute pharyngitis, 3 from peritonsillar abscesses, and 2 from odontogenic infection. Serious complications such as mediastinitis, cervical necrotizing fasciitis, sepsis accompanied by disseminated intravascular coagulation, and spondylitis of the cervical vertebrae were seen in 4 cases. Among organisms isolated, the S. milleri group appeared to be a pathogen contributing to abscess formation and to serious complications. The genus Streptococcus was most frequently isolated both in our 27 cases (66.7%) and the 200 in the literature (45.5%). Among species of the genus Streptococcus, the S. milleri group numbered the highest in our cases at 33.3% but only 8.5% in the literature. Cases in the literature, however, contained many unknown species of Streptococci--31.5% vs. 18.5% in our cases. alpha-streptococcus was frequently reported in the literature among unknown species of Streptococci--36 of 63. Culture-negative cases were also numbered more in the literature than in our case--29.0% vs. 18.5%. Special conditions and procedures are required to suitably isolate and detect the S. milleri group. Since not all facilities use identical techniques in routine bacteriological examination, a considerable number of the S. milleri group could be missed in unknown species of Streptococci or alpha-streptococcus and culture-negative cases. The detailed pathogenesis of the S. milleri group remains to be clarified. Infection by normal flora on mucosa is thought to occur due to an imbalance between organisms and host defense in deep neck abscesses. Some strains of the S. milleri group have been reported to produce many tissue-destroying enzymes such as collagenase and hyaluronidase. The co-existence of the S. milleri group with some anaerobe strains has also been suggested to accelerate inflammation. We discuss the mechanism inducing the massive release of cytokines through T cell response to certain exotoxins produced by S. milleri group, as reported in toxic shock-like syndrome due to the group A beta-streptococcus and in alpha-streptococcal shock syndrome due to viridans streptococci (alpha-streptococci).
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PMID:[Clinical and bacteriological significance of the Streptococcus milleri group in deep neck abscesses]. 1125 79

The inhibitors of hyaluronidase present in mammalian sera, first described half a century ago, have remained uncharacterized. Because of increased interest in hyaluronidases and their hyaluronan substrate, a study of these inhibitors was undertaken recently. The predominant serum inhibitor is magnesium-dependent and is eliminated by protease or chondroitinase digestion, and by heat. Kinetics of inhibition are similar against hyaluronidases from testis, snake and bee venom. The inhibitor has no effect on Streptomyces hyaluronidase; indicating inhibition is not through protection of the hyaluronan substrate. Circulating inhibition levels are increased in mice following carbon tetrachloride or interleukin-1 injection, inducers of the acute-phase response. Reverse hyaluronan gel zymography reveals a predominant band of 120 kDa relative molecular size. Additional studies indicate that the inhibitor resembles a member of the Kunitz type inter-alpha-inhibitor family. Inhibition of hyaluronidase activity is observed using purified inter-alpha-inhibitor and is reversed by antibodies specific for inter-alpha-inhibitor. This molecule, found in the hyaluronan-rich cumulus mass surrounding mammalian ova and the pericellular coat of fibroblasts and mesothelial cells, may function to stabilize such matrices by protecting against hyaluronidase degradation. Turnover of circulating hyaluronan is extraordinarily rapid, with a half-life of two to five min. Prompt increases in levels of serum hyaluronan occur in patients with shock, septicemia or massive burns, increases that may be partly attributed to suppression by these acute phase reactants of the constant and rapid rates of hyaluronan degradation by hyaluronidase. A literature survey of other hyaluronidase inhibitors is also presented.
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PMID:Inhibitors of the hyaluronidases. 1182 90

Circulating endotoxin is elevated in sepsis and plays a role in endothelial dysfunction whereas antithrombin is decreased by virtue of its consumption during complex formation with clotting factors and by proteolytic degradation by granulocyte elastase. Dysfunction of endothelium results in enhanced leukocyte rolling and diapedesis into tissues leading to edema formation and injury. Antithrombin exerts beneficial effects on endothelial function in sepsis. A direct anti-inflammatory action of anti-thrombin in inflammatory cells is exerted via heparan sulfate proteoglycans. In this study, we investigated whether antithrombin affects endotoxin-induced adhesion of neutrophils to human endothelial cells in vitro and whether glycosaminoglycans are involved in its signaling. Adhesion of human neutrophils to monolayers of umbilical vein endothelial cells was tested under static conditions. Endothelial cells were pretreated with endotoxin, interleukin-1, heparinase-I, chondroitinase-ABC or anti-syndecan-4-antibody. Endotoxin and interleukin-1 increased neutrophil adherence to human umbilical vein endothelial cells which was inhibited by antithrombin. Concomitant incubation with pentasaccharide abolished this effect of antithrombin. Treatment of endothelial cells with heparinase or chondroitinase led to higher adhesion and prevented effects of antithrombin. With antibodies to syndecan-4, enhanced adhesion of neutrophils was observed. As studied by Western blotting, endotoxin-induced signaling was diminished by antithrombin and the effect was reversible by chondroitinase or heparinase. From our results, we can conclude that endotoxin-induced adhesion of leukocytes to endothelium can be reversed by ligation of syndecan-4 with antithrombin's heparin-binding site and interferences with stress response signaling events in endothelium.
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PMID:Syndecan-4-dependent signaling in the inhibition of endotoxin-induced endothelial adherence of neutrophils by antithrombin. 1465 50

Agonistic and antagonistic peptides for formyl peptide receptor like 1 (FPRL1) receptor have been investigated as novel drug candidates for inflammatory diseases such as sepsis, asthma, and rheumatoid arthritis. In this work, a novel protocol for the synthesis of hyaluronic acid (HA)-peptide (CWRYMVm) conjugate for FPRL1 receptor was successfully developed for further clinical applications of peptide drugs. Aminoethyl methacrylated HA (HAAEMA) was synthesized by the coupling reaction of tetrabutyl ammonium salt of HA (HA-TBA) and AEMA using benzotriazol-1-yloxy-tris(dimethylamino) phosphonium hexafluorophosphate (BOP) in dimethyl sulfoxide (DMSO). Then, HA-AEMA was conjugated with CWRYMVm in water via Michael addition reaction between methacrylate group of HA-AEMA and thiol group in cysteine. The formation of HA-peptide conjugate was confirmed by 1H NMR and gel permeation chromatography (GPC). The average number of conjugated peptide molecules could be controlled from 5 to 23 per single HA chain. The HA-peptide conjugate showed serum stability longer than four days. In Vitro signal transduction activity of the HA-peptide conjugate for FPRL1 receptor was confirmed from the elevated levels of phospho-extracellular signal-regulated kinase (pERK) and calcium ion in FPRL1 overexpressing RBL-2H3 cells. The partially decreased biological activity of HA-peptide conjugates by the steric hindrance of HA was recovered after its degradation by hyaluronidase treatment.
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PMID:Signal transduction of hyaluronic acid-peptide conjugate for formyl peptide receptor like 1 receptor. 1900 92


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