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E. Abraham - One of the best experts on this subject based on the ideXlab platform.
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Effects of haemorrhage on Bacterial antigen specific pulmonary plasma cell function
Clinical & Experimental Immunology, 2008Co-Authors: A Robinson, E. AbrahamAbstract:Nosocomial pneumonia is frequent after haemorrhage and trauma, and often contributes to multiple organ system failure, morbidity and mortality in this setting. Although the percentages and numbers of Bacterial Polysaccharide antigen-specific pulmonary B cell clonal precursors are markedly decreased after haemorrhage, the effects of haemorrhage on pulmonary plasma cells actually producing antibody to these antigens are unknown. To investigate this question, the numbers of intraparenchymal pulmonary plasma cells producing antibody against the Bacterial Polysaccharide antigen levan (from Aerobacter levanicum) as well as Bacterial antigen specific secretory IgA (sIgA) titres in the lungs were determined at various time points after 30% blood volume haemorrhage. Reduced numbers of Bacterial antigen specific pulmonary plasma cells were found for more than 21 days following haemorrhage. An almost complete disappearance from the lungs of levan specific plasma cells occurred between 3 and 21 days after blood loss. Titres of Bacterial antigen specific sIgA in the lungs were decreased starting at 3 days post-haemorrhage and remained significantly depressed for more than 35 days after blood loss. These results demonstrate that haemorrhage produces profound and long-lasting suppression in Bacterial antigen-specific pulmonary plasma cell function. Because these effects do not occur immediately post-haemorrhage, immunization techniques able to enhance Bacterial antigen specific sIgA titres at pulmonary surfaces may be able to increase resistance to nosocomial pneumonia if administered shortly after injury and blood loss.
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Intranasal immunization with liposomes containing IL-2 enhances Bacterial Polysaccharide antigen-specific pulmonary secretory antibody response.
Journal of immunology (Baltimore Md. : 1950), 1992Co-Authors: E. Abraham, S ShahAbstract:Secretory IgA (sIgA) present at mucosal surfaces such as the lungs and intestine plays an important role in resistance to infection occurring at these anatomic sites. Because IL-2 and IL-4 can augment B cell proliferation and Ig production, we investigated possible adjuvant effects of these cytokines on Bacterial Polysaccharide-specific pulmonary sIgA generation. As shown in previous studies, intranasal immunization with liposomes containing Bacterial Polysaccharide from Aerobacter levanicum and Pseudomonas aeruginosa resulted in increased numbers of Bacterial Polysaccharide-specific pulmonary plasma cells and sIgA titers, compared with those found in unimmunized mice. Inclusion of IL-2, but not IL-4, into the intranasally administered liposomes further increased titers of Bacterial Polysaccharide specific sIgA and pulmonary plasma cells. Intranasal vaccination with liposomes containing Bacterial Polysaccharide and 10 micrograms/kg IL-2 increased Bacterial Polysaccharide-specific pulmonary plasma cell numbers by more than 80-fold compared with the response in mice immunized with liposomes containing Bacterial Polysaccharide, but without IL-2. The percentage of pulmonary plasma cells producing antibody to Polysaccharide from A. levanicum rose from 0.14% in mice intranasally immunized with liposomes containing only Polysaccharide to 4.1% in animals vaccinated with liposomes containing Polysaccharide and IL-2. Intranasal immunization with liposomes containing P. aeruginosa Polysaccharide and IL-2 significantly reduced mortality from P. aeruginosa pneumonia. These results demonstrate that IL-2 has potent adjuvant effects on Bacterial Ag-specific sIgA production in the lungs when included in intranasally administered liposomes.
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Modulation of the posthemorrhage Bacterial Polysaccharide antigen-specific antibody response by interleukins 2 and 4.
Lymphokine and cytokine research, 1992Co-Authors: E. Abraham, Yi-han ChangAbstract:Abnormalities in immune response play a major role in the increased susceptibility to infection after hemorrhage and trauma. Several studies have shown decreased release in vitro of interleukin-2 (IL-2) following blood loss. To better define in vivo the interactions between T and B cells, as well as the effects of treatment with the T cell-derived cytokines IL-2 and IL-4, mice were injected with concanavalin A at predetermined times posthemorrhage, and the percentages and numbers of splenic plasma cells producing antibody to the Bacterial Polysaccharide antigen levan (from Aerobacter levanicum) were determined. Decreased numbers and percentages of levan specific splenic plasma cells were found in animals treated with concanavalin A both immediately and 2 to 4 days after hemorrhage. Treatment in vivo with recombinant IL-2, but not IL-4 or anti-IL-2 receptor antibodies, following blood loss was able to increase the numbers of levan specific plasma cells to levels as high or higher than those found in normal, unhemorrhaged animals, but was unable to affect the decreased percentage of levan specific splenic plasma cells. These results suggest that the use in vivo of IL-2 may restore Bacterial antigen specific antibody responses to normal levels after blood loss.
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Effects of hemorrhage and resuscitation on Bacterial antigen-specific pulmonary plasma cell function
Critical Care Medicine, 1991Co-Authors: Anstella D. Robinson, E. AbrahamAbstract:BACKGROUND AND METHODS Nosocomial pneumonia is frequent after hemorrhage and trauma, and often contributes to multiple organ system failure, morbidity, and mortality in this setting. Although the percentages and numbers of resting pulmonary B cells (clonal precursors) able to be stimulated to produce antibodies to Bacterial antigens are markedly decreased after hemorrhage, the effects of hemorrhage on the pulmonary plasma cells actually producing antibody to Bacterial antigens have not been examined. To investigate this question, mice were bled 30% blood volume, then resuscitated with the shed blood 1 hr later. At predetermined times after hemorrhage, the mice were intranasally immunized with liposomes containing the Bacterial Polysaccharide antigen levan (from Aerobacter levanicum). One week later, lung lavages were performed to measure Bacterial antigen-specific secretory immunoglobulin A (sIgA) titers and the numbers of intraparenchymal pulmonary plasma cells producing antibody against the Bacterial antigen were determined. RESULTS Reduced numbers of pulmonary plasma cells producing antibody against the immunizing Bacterial Polysaccharide antigen were found between 1 and 14 days after blood loss, and titers of Bacterial antigen-specific secretory IgA were decreased for greater than 2 wks after hemorrhage. The importance of these abnormalities in pulmonary B-cell function was demonstrated by an increased susceptibility to Pseudomonas aeruginosa pneumonia in mice infected 4 days after hemorrhage, when Bacterial antigen-specific pulmonary plasma cell numbers were at their lowest point. Resuscitated mice showed the same increased susceptibility to P. aeruginosa pneumonia as did hemorrhaged but unresuscitated animals. CONCLUSIONS Hemorrhage, even if resuscitated, results in alterations in Bacterial antigen-specific pulmonary B-cell function and secretory IgA production that are profound, long lasting, and associated with increased susceptibility to infection at this mucosal surface. Because these effects on pulmonary B-cell function do not occur immediately after hemorrhage, immunization techniques able to enhance Bacterial antigen-specific secretory IgA titers at pulmonary surfaces may be able to increase resistance to nosocomial pneumonia if administered shortly after injury and blood loss.
John F Kearney - One of the best experts on this subject based on the ideXlab platform.
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limiting cdr h3 diversity abrogates the antibody response to the Bacterial Polysaccharide α 1 3 dextran
Journal of Immunology, 2011Co-Authors: Harry W Schroeder, Tamer I Mahmoud, John F KearneyAbstract:Anti-Polysaccharide Ab responses in mice are often oligoclonal, and the mechanisms involved in Ag-specific clone production and selection remain poorly understood. We evaluated the relative contribution of DH germline content versus N nucleotide addition in a classic oligoclonal, T-independent Ab response (α 1→3 dextran [DEX]) by challenging adult TdT-sufficient (TdT+/+) and TdT-deficient (TdT−/−) gene-targeted mice, limited to the use of a single DH gene segment (D-limited mice), with Enterobacter cloacae. D-limited mice achieved anti-DEX–specific levels of Abs that were broadly comparable to those of wild-type (WT) BALB/c mice. Sequence analysis of the third CDR of the H chain intervals obtained by PCR amplification of VH domain DNA from DEX-specific plasmablasts revealed the near universal presence of an aspartic acid residue (D99) at the V–D junction, irrespective of the composition of the DH locus. Although WT mice were able to use germline DH (DQ52, DSP, or DST) gene segment sequence, TdT activity, or both to produce D99, all three D-limited mouse strains relied exclusively on N addition. Additionally, in the absence of TdT, D-limited mice failed to produce a DEX response. Coupled with previous studies demonstrating a reduced response to DEX in TdT−/− mice with a WT DH locus, we concluded that in the case of the anti-DEX repertoire, which uses a short third CDR of the H chain, the anti-DEX response relies more intensely on sequences created by postnatal N nucleotide addition than on the germline sequence of the DH.
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generation of b cell memory to the Bacterial Polysaccharide α 1 3 dextran
Journal of Immunology, 2009Co-Authors: Jeremy B Foote, John F KearneyAbstract:B1b B cells generate a novel form of memory and provide Ab mediated-protection to persisting Bacterial pathogens. To understand how B1b B cells establish memory to Polysaccharide Ags, we studied an oligoclonal B cell response to α-1,3 dextran (DEX) expressed on Enterobacter cloacae. B cells specific for DEX enrich in the marginal zone (MZ) and B1b B cell populations. After E. cloacae immunization, MZ B cells were responsible for the generation of initial peak DEX-specific Ab titers, whereas, DEX-specific B1b B cells expanded and played an important role in boosted production of DEX-specific Ab titers upon E. cloacae rechallenge. Cell transfer experiments demonstrate that B1b B cells possess the capacity for both robust proliferation and plasma cell differentiation, thus distinguishing themselves from MZ B cells, which uniformly commit to plasma cell differentiation. These results define B1b B cells as the principal reservoir for memory to Bacterial-associated Polysaccharide Ags.
Cornelis P J Glaudemans - One of the best experts on this subject based on the ideXlab platform.
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binding of the o antigen of shigella dysenteriae type 1 and 26 related synthetic fragments to a monoclonal igm antibody
Journal of Biological Chemistry, 1993Co-Authors: Eugenia M Nashed, Pavol Kovac, Arthur B Karpas, R Schneerson, J B Robbins, Cornelis P J GlaudemansAbstract:where Rhap is rhamnopyranosyl, Galp is galactopyr- anosyl, and Glcp is glucopyranosyl. Using ligand-in- duced protein fluorescence change, we have measured the affinities of a monoclonal murine IgM for 26 frag- ments of, or related to, the structure of the O-polysac- charide and of the IgM Fab for the intact O-specific Bacterial Polysaccharide. Synthetic saccharides used were methyl glycosides to ensure an anomerically de- fined pyranosyl ring conformation. The galactosyl res- idue is the only monosaccharide of the antigenic epi- tope that shows quantifiable binding: -3.0 kcal/mol of binding free energy, depending on the structure and conformation of the fragment it is a part of. Addition of an a-(l+2)-linked rhamnosyl residue increases the free energy of binding significantly. We propose this rhamnopyranosyl-a-( 1+2)-galactopyranosyl disac- charide to be the basic determinant of the
A Robinson - One of the best experts on this subject based on the ideXlab platform.
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Effects of haemorrhage on Bacterial antigen specific pulmonary plasma cell function
Clinical & Experimental Immunology, 2008Co-Authors: A Robinson, E. AbrahamAbstract:Nosocomial pneumonia is frequent after haemorrhage and trauma, and often contributes to multiple organ system failure, morbidity and mortality in this setting. Although the percentages and numbers of Bacterial Polysaccharide antigen-specific pulmonary B cell clonal precursors are markedly decreased after haemorrhage, the effects of haemorrhage on pulmonary plasma cells actually producing antibody to these antigens are unknown. To investigate this question, the numbers of intraparenchymal pulmonary plasma cells producing antibody against the Bacterial Polysaccharide antigen levan (from Aerobacter levanicum) as well as Bacterial antigen specific secretory IgA (sIgA) titres in the lungs were determined at various time points after 30% blood volume haemorrhage. Reduced numbers of Bacterial antigen specific pulmonary plasma cells were found for more than 21 days following haemorrhage. An almost complete disappearance from the lungs of levan specific plasma cells occurred between 3 and 21 days after blood loss. Titres of Bacterial antigen specific sIgA in the lungs were decreased starting at 3 days post-haemorrhage and remained significantly depressed for more than 35 days after blood loss. These results demonstrate that haemorrhage produces profound and long-lasting suppression in Bacterial antigen-specific pulmonary plasma cell function. Because these effects do not occur immediately post-haemorrhage, immunization techniques able to enhance Bacterial antigen specific sIgA titres at pulmonary surfaces may be able to increase resistance to nosocomial pneumonia if administered shortly after injury and blood loss.
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Oral immunization with Bacterial Polysaccharide and adjuvant enhances antigen-specific pulmonary secretory antibody response and resistance to pneumonia.
Vaccine, 1991Co-Authors: Edward Abraham, A RobinsonAbstract:Abstract Nosocomial pneumonia, often due to Pseudomonas aeruginosa , occurs frequently after haemorrhage and trauma, and contributes to the increased incidence of morbidity and mortality in this clinical setting. In order to determine if enhancement of Bacterial antigen-specific secretory IgA (sIgA) titres in the lungs can increase resistance to P. aeruginosa pneumonia following haemorrhage, we investigated oral immunization strategies, using Bacterial Polysaccharides (levan, from Aerobacter levanicum , and P. aeruginosa Polysaccharide type I) and adjuvant (cholera toxin and the B-subunit of cholera toxin), capable of increasing Bacterial Polysaccharide-specific pulmonary secretory antibody titres. Oral co-administration of 1000 μg levan and 10 μg cholera toxin resulted in increased titres of levan-specific sIgA in lung lavages and increased numbers of levan-specific pulmonary plasma cells, but no changes in serum anti-levan titres. Similarly, oral co-administration of 1000 μg P. aeruginosa Polysaccharide and 10 μg cholera toxin produced increased anti- P. aeruginosa Polysaccharide titres in lung lavages. Significant decreases in anti-levan pulmonary sIgA titres and in numbers of levan-specific pulmonary plasma cells were found when oral immunization with levan and cholera toxin was performed 4 days following haemorrhage, but not if the mice were immunized 8 h after blood loss. Although haemorrhage markedly increased the susceptibility of mice to P. aeruginosa pneumonia, significant protection from mortality could be achieved through oral immunization with 1000 μg P. aeruginosa polysacccharide and 10 μg cholera toxin 8 h after haemorrhage. These results demonstrate that haemorrhage induces marked alterations in Bacterial antigen-specific pulmonary B-cell responses, which contribute to the increased susceptibility to infection in this setting. Oral immunization post haemorrhage with Bacterial Polysaccharides and adjuvant can improve resistance to pulmonary infection.
Yuriy A. Knirel - One of the best experts on this subject based on the ideXlab platform.
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the unique structure of Bacterial Polysaccharides immunochemical studies on the o antigen of proteus penneri 4034 85 clinical strain classified into a new o83 proteus serogroup
International Journal of Biological Macromolecules, 2020Co-Authors: Malgorzata Siwinska, Alexander S Shashkov, Agnieszka Zablotni, Evgeniya A Levina, Olga G Ovchinnikova, Antoni Rozalski, Yuriy A. KnirelAbstract:Abstract The serological classification scheme of the opportunistic Proteus bacilli includes a number of Proteus penneri strains. The tested P. penneri 4034-85 strain turned out to be serologically distinguished in ELISA and Western blotting. The O-Polysaccharide was obtained by mild acid degradation of the lipoPolysaccharide of this strain and studied by sugar and methylation analyses and dephosphorylation along with 1H and 13C NMR spectroscopy, including 2D 1H,1H COSY, TOCSY, ROESY, 1H,13C HSQC, HMBC, and HSQC-TOCSY experiments, The O-Polysaccharide was found to have a linear repeating unit containing glycerol 1-phosphate and two residues each of Gal and GlcNAc. The following O-Polysaccharide structure was established, which, to our knowledge, is unique among known Bacterial Polysaccharide structures: →4)-β- d -GlcpNAc-(1→3)-α- d -Galp-(1→3)-β- d -GlcpNAc-(1→2)-β- d -Galp-(1→3)-Gro-1-P-(O→.
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Structure of the O-Polysaccharide of Escherichia coli O60
Russian Chemical Bulletin, 2018Co-Authors: A. V. Perepelov, Alexander S Shashkov, Olesya I. Naumenko, S. N. Senchenkova, Alexander O. Chizhov, Yuriy A. KnirelAbstract:Structure of the O-Polysaccharide (O-antigen) of Escherichia coli O60 was studied by sugar analysis, partial solvolysis with CF3CO2H, and 1D and 2D 1H and 13C NMR spectroscopy. The O-Polysaccharide was found to consist of D-galactose and L-rhamnose. The structure of its branched tetrasaccharide repeating unit was established, which is unique among known Bacterial Polysaccharide structures.
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studies on the o specific Polysaccharide of the lipoPolysaccharide from the pseudomonas mediterranea strain c5p1rad1 a bacterium pathogenic of tomato and chrysanthemum
Carbohydrate Research, 2017Co-Authors: Evelina L Zdorovenko, Yuriy A. Knirel, Alexander S Shashkov, Alessio Cimmino, Guido Marchi, M Fiori, Antonio EvidenteAbstract:Abstract An O-specific Polysaccharide (OPS) was isolated from the lipoPolysaccharide of Pseudomonas mediterranea strain C5P1rad1, the causal agents of tomato pith necrosis and Chrysanthemum stem rot, and studied by one- and two-dimensional 1 H and 13 C NMR spectroscopy. The following structure of the trisaccharide repeating unit of the OPS was established, which, to our knowledge, is unique among the known Bacterial Polysaccharide structures: →4)-β- d -Man p NAc3NAcA-(1 → 4)-β- d -Man p NAc3NAcA-(1 → 3)-α- d -Qui p NAc4NAc-(1→ where QuiNAc4NAc and ManNAc3NAcA indicate 2,4-diacetamido-2,4,6-trideoxyglucose and 2,3-diacetamido-2,3-dideoxymannuronic acid, respectively. Pre-treatment of leaves with LPS or OPS preparations at 250 and 50 μg mL −1 did not inhibit development of a hypersensitivity reaction induced by P. mediterranea C5P1rad1 on tobacco, tomato and chrysanthemum plants. The same preparations at 250 μg mL −1 partially prevented elicitation of the hypersensitivity reaction by Pseudomonas syringae KVPT7RC on chrysanthemum but not tobacco and tomato.