Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0519030 (Klebsiella)
 21,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When Klebsiella pneumoniae capsular polysaccharide (CPS-K) from type 1, Kasuya strain, was injected intraperitoneally (i.p.) immediately before i.p. bacterial challenge, the survival time of mice infected with Salmonella enteritidis NUB 1 (virulent strain) was shortened and the mortality rate for mice infected with S. enteritidis NUB 31 (avirulent strain) was enhanced. The promotion of infection with S. enteritidis NUB 1 by CPS-K depended upon its dose, the effect of CPS-K being demonstrable up to as little as 0.2 mug per mouse. In the case of S. enteritidis NUB 31, the effect of CPS-K was detectable only when more than 20 mug per mouse was injected. As a result of enumeration of bacterial populations in the peritoneal washing, blood, liver and spleen, it was revealed that CPS-K promoted in vivo growth of S. enteritidis NUB 1 and NUB 31. In addition, CPS-K enhanced the mortality rate in mice infected with Streptococcus pyogenes or Streptococcus pneumoniae. The peak CPS-K effect on infection with S. enteritidis NUB 1 was seen when given immediately before bacterial challenge. The active substance responsible for the infection-promoting effect of CPS-K was neutral CPS-K, which is distinct from the O antigen and from acidic CPS-K (the type-specific capsular antigen). Preparations of neutral CPS-K isolated from the other three strains of K. pneumoniae exhibited a marked infection-promoting effect comparable with that of preparations from the Kasuya strain. Neutral CPS-K, with identical antigenicity to that from the Kasuya strain, has already been found to exert a strong adjuvant effect on antibody responses to various antigens in mice. No parallelism exists between infection-promoting activity and adjuvant activity of neutral CPS-K.
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PMID:Effect of capsular polysaccharide of Klebsiella pneumoniae on host resistance to bacterial infections. I. Induction of increased susceptibility to infections in mice. 0 28

Interferon production stimulated by the active substance (neutral fraction) of the capsular polysaccharide of Klebsiella pneumoniae (neutral CPS-K) in BCG-infected mice was compared with that by bacterial lipopolysaccharide (LPS). Prior infection with BCG increased the responsiveness of mice to the lethal effect of neutral CPS-K as well as to that of LPS. Associated with this, BCG-infected mice showed a markedly enhanced ability to produce interferon after stimulation not only by LPS but also by neutral CPS-K. In addition, a cytotoxic factor (cytotoxin) was found to be released in the serum of BCG-infected mice after injection of these inducers. The kinetics of production of interferon and cytotoxin stimulated by neutral CPS-K were very similar to those stimulated by LPS. The time pattern of cytotoxin production was not in parallel with that of interferon production. Interferon reached a peak 2 hr and cytotoxin 3 hr after injection with these inducers. Interferon and cytotoxin produced by neutral CPS-K showed essentially the same stabilities to heating at 56 C and to treatment at pH 2 respectively as those produced by LPS. Interferon was inactivated by heating at 56 C more rapidly than cytotoxin. Cytotoxin was inactivated by treatment at pH 2 for 24 hr, whereas interferon activity was well preserved after this treatment. These results suggest that both activities are the result of different substances.
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PMID:Interferon and cytotoxic factor (cytotoxin) released in the blood of mice infected with Mycobacterium bovis BCG. I. Enhanced production of interferon and appearance of cytotoxin stimulated by capsular polysaccharide of Klebsiella pneumoniae or bacterial lipopolysaccharide. 4 Nov 63

The capsular polysaccharide of Klebsiella pneumoniae (CPS-K) type 1, Kasuya strain, induces interferon production in the blood of mice when injected intravenously. CPS-K resembles bacterial endotoxin (lipopolysaccharide) in the time pattern of interferon production, with peak levels 2h after injection. CPS-K on a weight basis exhibits a more potent interferon-inducing effect than lipopolysaccharide. The active substance responsible for the interferon-inducing activity of CPS-K is the neutral CPS-K antigen which is antigenically distinct from the O antigen and from acidic CPS-K (the type-specific capsular antigen). Neutral CPS-K from the Kasuya strain has been already found to exhibit a strong adjuvant effect on antibody responses to various antigens in mice. Preparations of neutral CPS-K from other strains of K. pneumoniae, of which adjuvant action is only very weak, exhibit interferon-inducing activity similar to the preparation from the Kasuya strain. Heterologous and homologous tolerance to re-induction of interferon is produced by a prior injection (one each) of LPS, neutral CPS-K, and acidic CPS-K. No simple correlation exists between the inducing and tolerogenic capabilities of these substances.
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PMID:Interferon production in mice by the capsular polysaccharide of Klebsiella pneumoniae. 16 21

Using the capsular polysaccharide of Klebsiella pneumoniae (CPS-K) as a polyclonal B-cell activator (PBA) and sheep red blood cells (SRBC) as a T-dependent antigen, the correlation of the actions of PBA and T-dependent antigen on B cells in induction and amplification of immunological memory was studied. B-memory cell function, as judged by anti-SRBC responsiveness in vitro of spleen cells of CPS-K, was amplified by the secondary injection of SRBC into SRBC-primed mice, whereas it was decreased markedly by injection of CPS-K. When CPS-K was injected simultaneously with, or 1 or 2 days before the secondary injection of SRBC, B-memory cell function was also decreased markedly. On the other hand, CPS-K did not inhibit induction of B-memory cell function when injected simultaneouly with the primary injection of SRBC. However, CPS-K inhibited induction of B-memory cell function when injected 3 days before the primary injection of SRBC. The inhibition by CPS-K of amplification of B-memory cell function in response to SRBC when CPS-K was injected simultaneously with the secondary injection of SRBC occurred markedly in mice primed with SRBC 8 days or longer before the secondary injection, whereas it was not detectable in mice primed 3 days before. It is concluded that the CPS-K-mediated signal and the SRBC-mediated signal act competitively on the same subpopulations of B cells in induction and amplification of memory, and that the susceptibility of B cells to the CPS-K-mediated negative signal changes correspondingly with their maturation stage.
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PMID:Competition of the actions of antigen and polyclonal B-cell activator in the induction and amplification of B-memory cell function. 35 63

The mechanism for the infection-promoting effect of the capsular polysaccharide of Klebsiella pneumoniae (CPS-K) was investigated using the experimental system in which mice were infected intraperitoneally (i.p.) with a virulent strain of Salmonella enteritidis immediately after i.p. injection of CPS-K. In the peritoneal phagocytes of CPS-K-untreated control mice, approximately 70, 3, and 10% of phagocytized bacteria survived 6, 12, and 24 hr after challenge, respectively, when calculated from the ratio of the number of cell-associated viable bacteria, which was estimated by direct plate count, to the number of phagocytized bacteria, which was estimated by microscopic observation of stained smears. In contrast, almost all of the phagocytized bacteria were viable throughout the experimental period in mice treated with CPS-K. The electron microscopical findings of the phagocytes obtained 12 hr after challenge showed that in the cells of mice treated with CPS-K almost all of the phagocytized bacteria were morphologically intact, with some of them in the stages of cell division, whereas in those of untreated control mice, almost all of the phagocytized bacteria underwent digestive changes. When the reaction product of acid phosphatase was examined by electron microscopy in the phagocytes obtained 12 hr after challenge, the enzyme activity in the phagosomes was very low in mice treated with CPS-K in comparison with that in untreated control mice. Enzyme assays of the lysosomal and extralysosomal fractions of peritoneal cells obtained at various times after challenge also showed that release of acid phosphatase from the lysosomal fraction to the extralysosomal fraction after bacterial challenge was inhibited in peritoneal cells of mice treated with CPS-K.
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PMID:Effect of capsular polysaccharide of Klebsiella pneumoniae on host resistance to bacterial infections. III. Further study of its effects on interactions between peritoneal leukocytes and virulent Salmonella enteritidis. 38 55

The time course of the occurrence of hyperreactivity in interferon and cytotoxin responses to the active substance (neutral fraction) of the capsular polysaccharide of Klebsiella pneumoniae (neutral CPS-K) and bacterial lipopolysaccharide (LPS) and of the hyperreactivity to their lethal effects was followed after infection with BCG in SMA and ICR strains of mice. The duration of these hyperreactivities of BCG-infected mice depended on the inoculum doses of BCG. The time patterns of the hyperreactivity to the lethal effects of neutral CPS-K and LPS were similar in both strains of mice, although the maximum toxicity of LPS by the intraperitoneal route in BCG-infected mice on a weight basis was stronger than that of neutral CPS-K. Irrespective of inducer and mouse strain, the time pattern of the hyperreactivity to produce cytotoxin was similar to that of the hyperreactivity to produce interferon. The patterns for these phenomena when neutral CPS-K was used as an inducer were also similar to those when LPS was used. In ICR mice the hyperreactivity in interferon and cytotoxin responses to either neutral CPS-K or LPS decayed significantly earlier than the hyperreactivity to their lethal effects, whereas in SMA mice the occurrence of both types of hyperreactivities seemed to be associated. Therefore, it is suggested that the mechanism for the hyperreactivity in interferon and cytotoxin responses to neutral CPS-K or LPS in BCG-infected mice is not necessarily the same as that for the hyperreactivity to their lethal effects.
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PMID:Interferon and cytotoxic factor (cytotoxin) released in the blood of mice infected with Mycobacterium bovis BCG. II. Influence of time after BCG inoculation on production of interferon and cytotoxin by capsular polysaccharide of Klebsiella pneumoniae or by bacterial lipopolysaccharide and on hyperreactivity to their lethal effects. 38 56

The neutral fraction (neutral CPS-K) of Klebsiella pneumoniae capsular polysaccharide (CPS-K) from type 1, Kasuya strain, has already been reported as the active substance responsible for the strong adjuvant effect of CPS-K. The present results demonstrate that neutral CPS-K exhibits further common biological activities with lipopolysaccharide (LPS) isolated from Salmonella enteritidis. The intensity of the lethality in mice of neutral CPS-K by the intraperitoneal route is very similar to that of LPS. Its lethality for mice by the intravenous (i.v.) route is significantly stronger than that of LPS, because the degree of increase in the sensitivity to their lethality by i.v. challenge is smaller for LPS than for neutral CPS-K. The intensity of the pyrogenicity of neutral CPS-K in rabbits is approximately one-tenth of that of LPS as judged by the minimal pyrogenic doses and fever indices. The skin-preparatory potency of neutral CPS-K for the dermal Shwartzman phenomenon in rabbits is also approximately one-tenth of that of LPS compared on the basis of the minimal skin-preparatory doses. When injected i.v., neutral CPS-K exhibits a provocative effect on hemorrhagic reactions in skin sites prepared with neutral CPS-K or LPS.
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PMID:Adjuvant action of capsular polysaccharide of Klebsiella pneumoniae on antibody response. V. Further biological properties of the active substance. 78 3

Using the capsular polysaccharide of Klebsiella pneumoniae (CPS-K) as a polyclonal B-cell activator (PBA) and sheep red blood cells (SRBC) as a T cell-dependent antigen, we compared the ability of PBA and antigen to differentiate (generate antibody-forming cells, AFC) and proliferate (generate immunological memory) virgin B cells and B memory cells. In vitro CPS-K induced the differentiation of IgM virgin B cells, IgM B memory cells and IgG B memory cells to AFC, as well as or better than SRBC. The differentiation of B memory cells to AFC by CPS-K did not require the participation of macrophages or T cells, whereas the action of SRBC depended strictly upon the helper actions of these cells. The responsiveness to CPS-K and SRBC of normal and antigen-primed spleen cells as judged by anti-SRBC PFC responses in vitro was markedly decreased after stimulation of virgin B cells and B memory cells in vivo by CPS-K injection into normal or primed mice but greatly increased after the injection of SRBC. The decrease in the responsiveness to CPS-K of spleen cells from mice treated with CPS-K appeared principally due to exhaustion of the functions of B cells and B memory cells. From the present data it has been concluded that the signals required for the differentiation and proliferation of B cells of B memory cells are different from each other, the signal for differentiation being provided by either antigen (SRBC) or PBA (CPS-K), while the signal for proliferation only by antigen.
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PMID:Comparative studies on the actions of antigen and polyclonal B-cell activator in differentiation and proliferation of B-cells and B memory cells. 78 31

In normal mice, the total count of peritoneal leukocytes was markedly decreased after intraperitoneal (i.p.) injection of the capsular polysaccharide of Klebsiella pneumoniae (CPS-K) depending on the dosage injected. This decrease was mainly due to the depletion of macrophages, and a decrease in the number of lymphocytes occurred to a lesser extent. CPS-K in relatively smaller doses mobilized polymorphonuclear neutrophilic leukocytes (PMN) into the peritoneal fluid but it decreased them transiently in larger doses. In mice infected i.p. with a virulent strain of Salmonella enteritidis, there was an abundant emigration of PMN into the peritoneal fluid. When 200 mug of CPS-K was injected i.p. immediately before bacterial challenge, emigration of PMN was markedly delayed for 48 hr after infection. Associated with this suppressed emigration of PMN, the numbers of macrophages and lymphocytes in the peritoneal fluid were significantly less in mice treated with CPS-K than those in untreated control mice for 48 hr after infection. The numbers of both cell-associated and extracellular bacteria in the peritoneal fluid were markedly greater in mice treated with CPS-K than those in untreated control mice. In both in vivo and in vitro experiments, ingestion of bacteria by macrophages and PMN was not blocked by CPS-K or neutral CPS-K, the active substance responsible for the infection-promoting effect of CPS-K. It appeared that CPS-K somehow impaired the intraphagocytic bactericidal activity.
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PMID:Effect of capsular polysaccharide of Klebsiella pneumoniae on Host resistance to bacterial infections. II. Effects on peritoneal leukocytes of normal mice and mice infected with virulent Salmonella enteritidis. 79 33

With the use of the capsular polysaccharide of Klebsiella pneumoniae (CPS-K) as a powerful adjuvant, high precipitin responses could be induced in mice to syngeneic eyeball extracts and thyroid gland extracts which were normally nonimmunogenic. Only very weak responses were induced to eyeball extracts by Freund's complete adjuvant. Repeated administrations of the antigens mixed with CPS-K at time intervals of 30 days (more than twice for the eyeballs or more than three times for the thyroid glands) were required for induction of high precipitin responses. Antibody responses detectable by the immunofluorescent technique could be induced to syngeneic lymphoid tissue extracts by injecting the mixture of antigen and CPS-K more than five times at time intervals of 30 days. These findings suggest that repeated stimulation by autoantigens together with such a strong adjuvant as CPS-K can terminate natural tolerance against autoantigens.
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PMID:Microbial adjuvant and autoimmunity. I. Induction of antibody responses to syngeneic tissue extracts in mice treated with capsular polysaccharide of Klebsiella pneumoniae. 109 86


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