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D Bitter-Suermann

Publications and source records attributed to D Bitter-Suermann.

At least 73 records · Page 4Linked to original sources
PubMed1987

Influence of lysophospholipids and PAF on the oxidative burst of PMNL.

Lysophosphatidylcholine (LC), platelet activating factor (PAF) and its precursor lysophosphatidalcholine (LP) enhance O-2-release by polymorphonuclear leucocytes (PMNL) triggered by PMA whereas lysophospholipids with other polar headgroups fail to do so. The generation of these lysophosphatidylcholine-like molecules appears to represent an essential step in the activation of the oxidative burst of the PMNL triggered by PMA since inhibition of phospholipase A2 (PLA2) by p-bromophenacylbromide (BB) or mepacrine results in an inhibition of the O-2 release. This inhibition seems to be due to the reduced generation of the phospholipids studied as it could be reversed by LP. In addition, stimulation of the oxidative burst of the PMNL by the chemotactic stimuli, N-formyl-methionyl-leucylphenylalanine (FMLP), and the complement fragment C5a could also be significantly enhanced by LP as shown by chemiluminescence. However, the response to the phagocytic stimulus, opsonized zymosan (Zx), is not affected by LP. These data provide evidence for the participation of phospholipid metabolism in the initiation of the oxidative burst of PMNL induced by the soluble monomeric stimuli PMA, FMLP and C5a.

Acetophenones↗
PubMed1987

Serotyping and genotyping of encapsulated Escherichia coli K1 sepsis isolates with a monoclonal IgG anti K1 antibody and K1 gene probes.

Among infectious diseases caused by E. coli the capsular type K1 plays a predominant role. E. coli K1 isolates account for 80% of cases of E. coli neonatal meningitis and 30% of E. coli sepsis strains. Serotyping of K1 strains has conventionally relied upon the use of K1-specific bacteriophages or serum agar methods with polyvalent anti K1 serum. In the study present here, 187 E. coli sepsis isolates have been analysed for production of the K1 antigen using K1 phages, K1 serum agar plates and Latex agglutination and ELISA using an IgG2a anti K1 monoclonal antibody. In total, 33 sepsis isolates (about 18%) were identified as K1 positive, with three of these strains proving negative in all tests except those exploiting the monoclonal antibody. That these three strains elaborate the K1 antigen was confirmed by Southern blot experiments using cloned K1 antigen production genes as probes. The failure of the three strains in all the tests except those that use monoclonal antibody could be explained by apparent disruption of K1 gene sequences that encode functions essential for the export of capsular material to the cell surface. The superiority of tests based on monoclonal antibodies above the conventional methods for detection of K1 antigen is evident.

Antibodies, Monoclonal↗
PubMed1987

Polysialic acid units are spatially and temporally expressed in developing postnatal rat kidney.

We report the presence of alpha(2----8)-linked polysialic acid as detected with a monoclonal antibody outside the nervous tissue in the postnatal developing rat kidney. By immunoblot analysis, the reactivity was confined to a broad band of apparent molecular mass 200-250 kDa. By immunohistochemistry, the polysialic acid units were found throughout the ureteric bud-derived collecting duct system. In developing nephrons derived from the metanephrogenic mesenchyme, polysialic acid units were only regionally and transiently expressed. Furthermore, the expression of polysialic acid units was developmentally regulated, as evidenced by their gradual disappearance concomitant with postnatal kidney maturation. These findings suggest a possible role for polysialic acid units in cell-cell contact-mediated renal differentiation processes.

Aging↗
PubMed1987

Qualitative and quantitative determination of enterobacterial common antigen (ECA) with monoclonal antibodies: expression of ECA by two Actinobacillus species.

The presence and quantity of the enterobacterial common antigen (ECA) in several species belonging to the family Enterobacteriaceae as well as to other gram-negative families were determined by a solid-phase enzyme-linked immunosorbent assay system and Western blotting by using mouse monoclonal antibodies specific for ECA. Except for Erwinia chrysanthemi, previously known to be an exception, all species known or presumed to belong to Enterobacteriaceae produced ECA (89 of 90 species). Most species not belonging to Enterobacteriaceae did not produce ECA (25 of 28 species), with one already known (Plesiomonas shigelloides) and two hitherto unknown (Actinobacillus equuli and Actinobacillus suis) exceptions. Interestingly, all strains of P. shigelloides produced ECA, regardless of the presence of the Shigella sonnei cross-reacting O antigen. Quantitation of the amount of ECA in members of the family Enterobacteriaceae revealed a remarkable heterogeneity among genera and species as well as within one species. We conclude that the rapid, sensitive, and reliable determination of ECA is a useful aid in taxonomic classification and may help to characterize the relatedness of the family Enterobacteriaceae to other families. However, a quantitative analysis of ECA appears to be without value for these purposes.

Actinobacillus↗
PubMed1987

Guillain-Barré syndrome: activated complement components C3a and C5a in CSF.

Plasma and spinal fluid levels of complement activation products C3a and C5a were quantitated by radioimmunoassay in a group of 16 patients suffering from acute monophasic Guillain-Barré syndrome (GBS). Median CSF levels of C3a (118 ng/ml) and of C5a (9.6 ng/ml) were significantly elevated when compared with samples from a control group of patients with noninflammatory neurologic diseases. Plasma concentrations of these anaphylotoxic peptides were not significantly different between the two populations. Our findings indicate that the complement system is activated in the CSF of patients with acute GBS. Complement activation products may contribute to the inflammatory changes observed in this disorder.

Complement C3↗
PubMed1986

The role and mechanism of cobra venom factor-induced suppression of the humoral immune response in guinea pigs.

The cobra venom factor (CVF)-mediated suppression of the humoral immune response to bacteriophage phi X 174, a T cell-dependent antigen, was investigated in guinea pigs. The suppression was markedly dependent on the amount of antigen used: decomplementation of animals diminished the humoral immune response when immunizing with low doses of antigen, whereas increasing the antigenic dose resulted in little or no diminution by CVF. In contrast to the results with normal animals, CVF had no influence on the humoral immune response of genetically C2-deficient guinea pigs; i.e., no suppression occurred above that due to the inherited complement deficiency state alone. We therefore postulate that CVF suppresses the humoral immune response by the depletion of C3, with no measurable role for complement split products under these experimental conditions.

Animals↗
PubMed1986

Interference of a C3-fragment preparation with IL 2-dependent proliferation.

A C3-fragment preparation (C3-FP) was studied for its ability to regulate human peripheral blood lymphocyte activation. It was found that very low concentrations of this low m.w. fraction, which was free of C3a, inhibited the PHA-induced lymphocyte proliferation without any cytotoxicity. Cytofluorometric analysis showed that C3-FP did not influence the transition of T cells from the G0 to the G1a phase of the cell cycle. However, the IL 2-dependent transition from the G1a to the G1b phase of the cell cycle was effectively blocked. Addition of exogenous IL 2 did not release cells arrested in the G1a phase. Furthermore, neither IL 2 production nor IL 2 receptor formation was inhibited by C3-FP, and binding of IL 2 to its receptor was unaltered. It was found that only IL 2-dependent cell lines were inhibited in their proliferation; all other tested cell lines were unaffected by C3-FP. Our findings suggest that cleaved products of C3 may inhibit IL 2-dependent lymphocyte proliferation at a stage where the IL 2 signal is required for initiation of proliferation.

Complement C3↗
PubMed1986

An inherited deficiency of the third component of complement, C3, in guinea pigs.

Hereditary deficiency of the third component of complement, C3, is found very seldom in the human. C3 deficiency is associated with severe bacterial infections revealing the central role of C3 in complement activation via the classical or alternative pathway. We describe a new hereditary C3 deficiency in strain 2 guinea pigs. Serum from these animals had a markedly reduced lytic activity in a standard assay for complement-dependent, antibody-mediated cytotoxicity. In functional assays of individual components, the hemolytic activity of the components C4, C2, C5 and of factors B, D and H was in the normal range. The functional C3 titer, and similarly C3 antigenic activity in the serum of these C3-deficient animals (C3D) was on average only 5.7% of normal activity. Typing the animals with alloantisera or monoclonal antibodies to guinea pig Ia-antigens revealed that the C3D animals had the major histocompatibility complex-haplotype of inbred strain 2 guinea pigs (B.1, Ia.2,4). The C3 defect is not linked to the major histocompatibility complex and, in addition, is not linked to a C3a receptor deficiency. Macrophages and hepatocytes of the C3D animals have an unimpaired capacity for synthesis and secretion of C3 as measured by enzyme-linked immunosorbent assay. There was no indication for hypercatabolism of normal C3 by the animals as shown by plasma clearance of 125I-radiolabeled C3. Thrombocytes of the C3D animals responded normally to stimulation with purified C3a in an ATP-release assay without an indication for a desensitization in vivo. Possibly the fault resides in an enhanced susceptibility of their own C3 to proteolysis. However, C3 partially purified from the plasma of the C3D animals or secreted by hepatocytes exhibited no obvious structural differences to purified normal C3 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis or in immunoblotting. The C3D serum had a reduced bactericidal activity compared to normal or to C4-deficient serum. Nevertheless, the animals are apparently healthy without an indication for increased frequency of bacterial infections. These guinea pigs provide an unique model for analysis of the biological functions of C3 in vivo and in vitro without the need for artificial C3-depletion procedures with all their known and unknown side-effects.

Animals↗
PubMed1986

Impaired humoral immune response in complement C3-deficient guinea pigs: absence of secondary antibody response.

A recently described genetically controlled C3 deficiency (C3D) in guinea pigs (GP) provided a unique model for studying the role of C3 in the afferent limb of the humoral immune response in a direct manner. These C3D animals, which have only 5-7% of normal serum C3 level, were immunized with the bacteriophage phi chi 174, a T cell-dependent antigen, followed by a booster injection after 4 weeks (1.5 X 10(9) plaque-forming units/kg). The formation of IgM and IgG antibody in the course of the primary and secondary response was determined and compared with a control group of inbred strain 2 GP. The C3D animals showed a markedly diminished antibody response to this antigen. Amplification of the antibody titer as well as regular isotype switching from IgM to IgG was absent in the secondary response. Increasing the amount of antigen to a high dose (1 X 10(10) plaque-forming units/kg) led to a normalization of the antibody response. The impairment in antibody formation resembles closely the impaired antibody response in C4-deficient or C2-deficient GP, which both have a block in activation of C3 via the classical pathway. However, in contrast to C4D GP or C2D GP the C3D GP do not exhibit serological characteristics of immune complex disease. They have normal levels of total serum IgM, of IgM anti-2,4-dinitrophenyl antibodies and of IgM rheumatoid factors.

Animals↗
PubMed1986

Evaluation of low dose anaphylatoxic peptides in the pathogenesis of the adult respiratory distress syndrome (ARDS). Monitoring of early C5a effects in a guinea-pig in vivo model after i.v. application.

A guinea-pig in vivo model is presented that allows the infusion of purified C5a via a central vein catheter and the monitoring of its effects on granulocytes and platelets, the most important cells in the pathogenesis of several lung disorders, e.g. shock lung. After the infusion of C5a, which was adjusted to a quantity that caused slight and transient alterations of lung physiology, granulocytes disappeared from circulation within 1 min. Simultaneously the granulocyte content of the lung increased about three-fold as judged by histological evaluations. Morphologic destructions were not observed. After the drop a rebound of circulating Polymorpho-nuclear leucocytes (PMN) occurred, which was significantly higher than control values and the appearance of banded cells indicated a mobilization from bone marrow stores. Studies with 51-chromium labelled PMNs revealed that most, but not all, of the granulocytes returned to circulation after transient sequestration. The number of platelets also decreased after C5a infusion, but the rebound was delayed compared with the PMNs and did not exceed control values. The changes in circulating cells, lung histology, and lung physiology are comparable to those occurring during the onset of shock lung and thus strengthen the supposed importance of C5a concerning the pathogenesis of that syndrome.

Animals↗
PubMed1986

Immunocytochemical localization of enterobacterial common antigen in Escherichia coli and Yersinia enterocolitica cells.

Enterobacterial common antigen (ECA) was localized on Lowicryl K4M sections and on ultrathin cryosections by using either a mouse monoclonal antibody or an absorbed rabbit polyclonal immune serum with the corresponding gold-labeled secondary antibodies. Comparable results were obtained with both monoclonal antibody and polyclonal immune serum. Controls with two ECA-negative mutants revealed the ECA specificity of both labeling systems. On Lowicryl K4M sections, good labeling of the outer membrane and of membrane-associated areas in the cytoplasm was obtained. Unexpectedly, however, the ribosome-containing areas of the cytoplasm also showed significant labeling. On ultrathin cryosections, labeling of the cytoplasmic areas was much weaker, although the density of label in the outer membrane was comparable to that obtained with the Lowicryl K4M sections. With the techniques used, it cannot be completely excluded that the appearance of ECA in the cytoplasm is due to displacement of ECA-reactive sites during the preparation procedure.

Antigens, Bacterial↗
PubMed1986

Molecular cloning and analysis of genes for production of K5, K7, K12, and K92 capsular polysaccharides in Escherichia coli.

With a DNA fragment from within the region encoding the transport functions for K1 production as a hybridization probe in Southern blot experiments, homologous DNA sequences were detected in the DNA from Escherichia coli strains producing K5, K7, K92, and K100 capsular polysaccharides. No homology with the laboratory strain LE392 was detected. The same DNA probe was used to prescreen cosmid libraries in LE392 by colony hybridization, as a rapid method to isolate clones encoding the genes for K5, K7, K12, and K92 antigen production. Clones carrying sequences homologous to the probe that also produced capsular material were identified by using polyclonal and monoclonal antibodies raised against the K antigen in question and K antigen-specific phages. By restriction enzyme mapping of the appropriate cosmid clones it was possible to align the genes for the production of different K antigens in terms of common restriction endonuclease cleavage sites. A DNA fragment encoding the postulated transport functions for K7 antigen production could complement deletion mutations in the transport functions for K1 antigen production. Thus the transport to the cell surface of chemically distinct polysaccharides may be by a common process. Analysis in E. coli of the proteins produced by plasmids carrying the likely transport functions for K1, K5, and K7 antigen production revealed that each region coded for a similar polypeptide.

Antigens, Bacterial↗
PubMed1986

Guinea pigs with inherited deficiencies of complement components C2 or C4 have characteristics of immune complex disease.

Guinea pigs genetically deficient in the second (C2) or fourth component of complement (C4) generally appear healthy in contrast to humans with a C2 or C4 deficiency. However, upon investigation of these genetic deficiencies in guinea pigs for signs of dysregulation in the humoral immune system and especially autoantibodies, many complement-deficient guinea pigs (greater than 50%) had elevated levels of serum IgM and higher concentrations of anti-hapten (dinitrophenyl) antibodies as signs of polyclonally stimulated antibody synthesis. In addition, a significant number of the complement-deficient animals, on average 30%, had IgM rheumatoid factors in their sera compared with less than 1% of the normal animals. These observations, therefore, indicate that guinea pigs, genetically deficient in C2 or C4, show characteristics of immune complex disease in general.

Aging↗
PubMed1986

Mediator systems in a passive model of in situ immune complex glomerulonephritis. Role for complement, polymorphonuclear granulocytes and monocytes.

The pathogenetic roles of complement, polymorphonuclear granulocytes, and monocytes were studied in a model of in situ immune complex glomerulonephritis employing a cationized antigen. Left kidneys of Wistar rats were perfused with 40 micrograms of cationized human IgG (isoelectric point greater than or equal to 9.5) followed by intravenous injection of rabbit anti-human IgG 1 hour later. This resulted in prominent subepithelial deposit formation in the perfused kidney accompanied by massive proteinuria. Groups examined were: (a) no additional treatment, (b) C3 depleted (cobra venom factor, (c) granulocyte depleted (specific antiserum), (d) monocyte depleted (specific antiserum), and (e) granulocyte depleted and monocyte depleted. The quantity of radiolabeled cationized antigen deposited in the left kidney was not affected by any of the treatment schedules. Proteinuria was abolished in all mediator depleted groups (b to e) for 5 to 7 days, thereafter rising to levels seen in the nondepleted group (a). This late onset of proteinuria is noteworthy since the deposits are then located subepithelially and may be less accessible to circulating mediators. C3 depletion, despite inhibition of proteinuria, did not prevent the intraglomerular accumulation of granulocytes and monocytes thereby suggesting that attraction and activation of these cells may occur independently. Apparently all three mediators are required for full expression of the lesion, a finding not paralleled in other experimental models of glomerulonephritis. The relevance of very low levels of inflammatory cell infiltration for provoking glomerular injury was clearly demonstrated.

Animals↗
PubMed1985

[Recurring meningococcal meningitis in hereditary C 5 deficiency].

Inherited deficiency of the 5th complement component (C5) was the cause of recurrent meningococcal meningitis in a woman aged 20 years. Familial investigations confirmed an autosomal co-dominant type of inheritance for the defect. Whereas additional loss of chemotaxis only exists with a genetic defect in C5 complement, bacteriolytic activity of serum is lacking in all genetic defects of the terminal complement components C5 to C8. An intact bacteriolysis, however, is necessary for resistance against Neisseria meningitidis and Neisseria gonorrhoeae. Neisseria infections, particularly recurrent meningococcal meningitis or disseminated gonococcal infections, suggest the presence of a congenital or acquired deficiency in one of the complement components C5 to C8.

Adult↗