[Influenza-bacillus: who discovered the organism?].
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Animals↗
Biomedical subjects
T Saito-Taki
Publications and source records attributed to T Saito-Taki.
[Newly developed MRSA medium].
We have developed a new selective medium, tentatively named MR(SA)2, for rapid identification of methicillin-resistant Staphylococcus aureus (MRSA) from clinical specimens. MR(SA)2 medium contained modified Müller-Hinton agar supplemented with 75 g of NaCl, 10 g of mannit, 20 mg of bromcresol purple, 20 g of egg-yolk, 4 mg of oxacillin, and 12.5 mg of ceftisoxime per 1,000 ml. There were no differences between the growth of MRSA strains on this medium at 30 C and that of 37 C. This medium can detect the egg-yolk reaction instead of the coagulase reaction. By single streaking of a test material on the surfaces of MR(SA)2 agar, MRSAs can easily be distinguished from methicillin-resistant coagulase-negative staphylococci (MR-CNS), other bacteria and fungi from their colony morphologies in a quantitative manner. A few MRSA strains would not form colonies on this medium because of their susceptibilities to ceftisoxime, but this may not inpede its use, since most MRSA strains isolated from clinical materials showed resistance to ceftisoxime. From the above results, the MR(SA)2 medium may be suitable for rapid detection of MRSA and MR-CNS.
Ceftizoxime↗
[Proposal for the nosocomial infection control of methicillin-resistant Staphylococcus aureus (MRSA)].
To determine the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) in hospital environments, quantitative isolation of MRSA from environmental and human specimens was performed. It was found that as many as 6 x 10(4) colony forming units (CFU)/100cm2 of MRSA and also methicillin-resistant coagulase-negative Staphylococcus (MRCNS) were isolated from 1) 25-100% of the bed-mattresses tested in 10 out of 11 (90%) hospitals, and also 2) bed sheets for patients, floors of patient wards, laundry, bath-room, toilet and laundry storage-room. And seven and eight palms of 20 patients were contaminated with MRCNS and MRSA, respectively, and MRCNS contamination was revealed in six of medical staffs. These results indicate that hospital environments, especially the mattresses and hospital floors are highly contaminated with MRCNS and MRSA, and sanitation and cleanliness of mattresses and floors are necessary to prevent the dissemination of both MRCNS and MRSA in hospital.
Cross Infection↗
Protective effect of cytokines in mice to Pseudomonas aeruginosa infection.
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Animals↗
IgG2b-dependent down regulation of the LPS-induced PFC-response and its blockade by Fc gamma 2bR protein.
Fc gamma receptor (Fc gamma R)-dependent immunoregulation by murine heat-aggregated (HAgg) IgG subclasses on the bacterial lipopolysaccharide (LPS)-induced plaque forming cell (PFC) response to trinitrophenylated sheep red blood cell (TNP-SRBC) antigen and the competitive effect by Fc gamma 2bR-protein on the down regulation by HAgg-IgG2b were studied in murine T-cell-deprived spleen cell cultures. HAgg-IgG1 and HAgg-IgG3 enhanced the PFC response, but HAgg-IgG2b strongly suppressed the LPS-induced PFC response. HAgg-IgG1 could not compete with the suppressive effect of HAgg-IgG2b. The HAgg-IgG2b seemed to act on both macrophages (M phi) and B-cells, because the cell cultures that had been reconstituted with HAgg-IgG2b-pretreated M phi and untreated B-cells and vice versa showed poor PFC responses. The suppression induced by HAgg-IgG2b on the LPS-induced PFC response in the T-cell-deprived cultures was abolished by the addition of phospholipase C (PLC)-treated Fc gamma 2bR protein at the early stage of the culture. The mechanisms by which HAgg-IgG2b suppress the LPS-induced PFC response and PLC-treated Fc gamma 2bR protein restores this response were discussed.
Androgen-Binding Protein↗
The adjuvant effect of a muramyl dipeptide (MDP) analog on temperature-sensitive Salmonella mutant vaccine.
Adjuvant effect of a synthetic muramyl dipeptide analog, MDP-Lys (L18), MurNAc-L-Ala-D-glu[Lys(CO-(CH2)16-CH3)-OH]NH2 on a live Salmonella enteritidis vaccine, a temperature-sensitive mutant Ts-O strain that was obtained from the virulent S. enteritidis No.11 strain and could not grow at 37 degrees C, but could multiply at 25 degrees C as fast as the parent strain, was examined. Although the Ts-O organisms were avirulent and could hardly multiply in vivo when the organisms were injected into C57BL/6 mice and its mutant beige strain, which has a malfunction of phagocytic cells, injection of these mice with Ts-O endowed them with some protective immunity against infection by the virulent No.11 strain. When MDP-Lys(L18) was injected with Ts-O vaccine, the protection and the bactericidal capacity in the peritoneal cavities and spleens of these mice were augmented. MDP-Lys(L18) was still effective when it was injected at 48 h before or after the inoculation of Ts-O vaccine. Its effect was also observed against infection by the virulent S. cholerae-suis Hokkaido strain, a strain that does not share common O-antigenic determinants with the S. enteritidis No.11 or Ts-O strain. In addition, the mice that were inoculated simultaneously with Ts-O organisms and MDP-Lys(L18) were examined 10 days later for their footpad delayed type hypersensitivity reactions against Ts-O antigen. Mice inoculated with MDP-Lys(L18) and Ts-O showed augmented footpad swelling in comparison with the controls. These findings indicate that MDP-Lys(L18) is capable of augmenting the cellular immunity by live vaccine.
Acetylmuramyl-Alanyl-Isoglutamine↗
Phagocytosis and bactericidal action of mouse peritoneal macrophages treated with leukotriene B4.
The effects of exogenous leukotriene B4 (LTB4) on the resistance of mouse peritoneal macrophages against Salmonella (S.) typhimurium and Pseudomonas (P.) aeruginosa infections were studied. In vitro, LTB4 added to macrophage monolayers at final concentrations of 10(-12)-10(-8) M, enhanced their phagocytosis of S. typhimurium to 2.3 times the control level and that of P. aeruginosa to 1.8 times the control level. The intracellular killing rates were also elevated by the addition of LTB4: for S. typhimurium, 83.3% (LTB4) vs 59.1% (control) and for P. aeruginosa, 46.5% (LTB4) vs 9.2% (control). In vivo, intraperitoneally injected LTB4 (5 ng) enhanced the clearance at 24 h of intraperitoneally injected S. typhimurium from the mouse peritoneal cavity (2.38 x 10(3) +/- 0.94 x 10(3) cells [LTB4] vs 5.73 x 10(5) +/- 1.90 x 10(5) [control]) and spleen (5.00 x 10(2) +/- 0.94 x 10(2) [LTB4] vs 2.47 x 10(4) +/- 0.84 x 10(4) [control]), but this effect disappeared by 48 h. In contrast, in beige mice, an experimental model of the Chédiak-Higashi syndrome that is characterized by susceptibility to bacterial infection, there was no induction of the eliminating effect by intraperitoneal injection of LTB4. Activation of macrophages by exogenous LTB4 seemed to have contributed to such an augmented resistance of macrophages to bacterial infection. This study suggested a possible use of LTB4 in bacterial infectious diseases whereby phagocytes are able to play a key role in host defense.
Animals↗
Toxicity of Microcystis aeruginosa K-139 strain.
Toxicity of the cells of a newly established axenic Microcystis aeruginosa K-139 strain to mice was studied. LD50 of the cells harvested in the mid-log phase was 7.3 mg/kg. The organs of acute dead mice were examined histopathologically. The blood congestion and necrosis of the parenchymal cells around the central veins in the liver were observed, but other organs seemed to be normal. The liver damage was confirmed by the tests of glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) activities in the sera of the mice after the injection with the K-139 cells. Furthermore, the K-139 cells were capable of inducing interleukin 1 (IL-1) production by peritoneal macrophages in vitro.
Animals↗
Enhanced bactericidal activity of macrophages by exogenous leukotriene B4.
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Animals↗
Study of the biological activities of toxic shock syndrome toxin-1: II. Induction of the proliferative response and the interleukin 2 production by T cells from human peripheral blood mononuclear cells stimulated with the toxin.
Toxic shock syndrome toxin-1 (TSST-1) is an exotoxin produced by Staphylococcus aureus isolated from patients with toxic shock syndrome. We investigated the proliferative response of human lymphocytes and their interleukin 2 (IL-2) production after stimulation with TSST-1 in vitro. Human cord blood mononuclear cells (HCBM) and human peripheral blood mononuclear cells (HPBM) could proliferate with TSST-1 stimulation. T cell-depleted HPBM showed only a marginal response to this toxin. A IL-2-like factor with a molecular weight of 15-18 kD was obtained from the supernatants of TSST-1-stimulated HPBM cultures. The factor was absorbed by CTLL-2 cells but not by T cell-depleted murine spleen cells, indicating that it is IL-2. HPBM are very sensitive to TSST-1: a low concentration of TSST-1 (0.01 ng/ml in 36 h stimulation) and a short period of stimulation (8 h at 10 ng/ml of the toxin) were fully effective for HPBM to produce substantial amounts of IL-2. Removal of T cells abrogated the TSST-1-induced IL-2 production by HPBM. Reconstituted cell cultures of nylon wool column-passed T cells and macrophages produced IL-2 by TSST-1 stimulation and, furthermore, the accessory activity of the macrophages could be partially replaced by a macrophage-derived factor containing interleukin 1. These findings indicate that T cells require macrophages or IL-1 for TSST-1-induced production of IL-2. The roles of lymphokines, including IL-2, in the development of this illness are discussed.
Bacterial Toxins↗
Serological determinants of fluorescent granular perithelial cells along small cerebral blood vessels in rodent.
As reported previously, the perivascular cells laden with fluorescent granules (FGP cell) are situated in Virchow-Robin space and show marked uptake capacity for intraventricularly administered substances. The phagocytic FGP cells are derived developmentally form leptomeningeal cells and are recognizable in various kinds of animals, including humans. In the present paper, the FGP cells of rodents are studied by immunological techniques. It is clearly demonstrated that rat FGP cells express the antigenic determinant for Ia antibody at about 7 days after birth, and also that mouse FGP cells show a positive reaction against mouse Fc and splenic macrophage antibodies at about the same developmental stage. The specific determinants of FGP cells appear concurrently with the initiation of horseradish peroxidase uptake. On the other hand, Ia antigen is also shown in subarachnoid macrophages, but not in immature FGP cells, endothelium and pericyte. Based on these findings, it seems reasonable to consider that the FGP cells are indigenous cerebral macrophages and significant for the local immune response in a cerebral tissue. Further, in this paper, to prevent confusion of the FGP cell with the other perivascular cells, the authors propose designating the FGP cell as Mato cell.
Aging↗
Genetic control of delayed-type hypersensitivity in mice to Salmonella antigen.
Genetic restriction on the expression of delayed-type hypersensitivity (DTH) to Salmonella typhimurium in mice transferred passively with immune spleen cells was studied. After the intravenous transfer of immune C3H/HeJ (H-2Ik) cells into A.TL (H-2Ik) or A.TH (H-2Is) mice, footpad DTH responses could be evoked in the A.TL recipients, but not in the A.TH mice. When the immune cells of BALB/c or C3H/He mice were intravenously-transferred into F1 hybrids produced by mating BALB/c and C57BL/6 or C3H/He and C57BL/6, respectively, no DTH response could be evoked in these F1 hybrids that received immune parental cells. Local transfer as well as systemic intravenous transfer of immune parental cells to F1 haplotype recipients did not cause any DTH. Previous treatment of the F1 hybrid recipients with cyclophosphamide did not result in the expression of the DTH response. Transfer of immune F1 spleen cells into parental strains also did not induce DTH. When the immune cells of parental strains were transferred into F2 mice and into back-cross mice, examination of the DTH response in these mice showed that some of them did not have any obvious footpad swelling, while others revealed various magnitudes of swelling. The resistance of F1 hybrids to transfer of DTH is discussed.
Animals↗
Comparison of murine B cell clonal expansions by synthetic lipid A and muramyl dipeptide analogs.
Direct stimulations of murine B lymphocytes with synthetic lipid A analogs and synthetic muramyl dipeptide (MDP) derivatives were studied using a limiting dilution assay system. Synthetic lipid A analogs, GLA-27 and GLA-40, when conjugated with bovine serum albumin (BSA) had the ability to induce B cell clonal expansion of a single B cell from the spleen or bone-marrow. Their activities were almost the same as those of naturally obtained lipid A, but were lower than that of bacterial lipopolysaccharide (LPS). Addition of dextran sulfate (DXS) enhanced the effect of lipid A analogs. In contrast, synthetic MDP and its derivatives, although they had many biological and immunological activities in experimental animals, could not stimulate a single B cell to induce clonal expansion regardless of the presence or absence of DXS. These results suggested that lipid A analogs can directly cause the proliferation of B cells, but MDPs can not.
Acetylmuramyl-Alanyl-Isoglutamine↗
Phospholipase A2 activity of Fc gamma 2b receptors of thioglycollate-elicited murine peritoneal macrophages.
The detergent lysate of plastic adherent cell population of thioglycollate-elicited peritoneal exudate cells from 100 individual Swiss mice was subjected to affinity chromatography on two different media, Sepharose coupled to heat-aggregated human IgG (IgG-Sepharose) and Sepharose coupled to the phosphatidylcholine analog, rac-1-(9-carboxyl)nonyl-2-hexadecylglycero-3 -phosphorylcholine (PC-Sepharose). Both IgG- and PC-binding proteins were further purified by Sephadex G-100 gel filtration and isoelectric focusing in the presence of 6M urea. Both IgG- and PC-binding proteins thus purified appear to be homogeneous in size as well as charge properties. The IgG-binding proteins of a molecular weight of 25,000 had an isoelectric point of 4.8, whereas the PC-binding proteins of a molecular weight of 42,000 were more basic and had an isoelectric point of 6.0. Both materials retained their IgG-binding capabilities as judged by their inhibitory capacity of murine EA gamma rosetting systems. The subclass specificities of the IgG- and the PC-binding proteins were for IgG2a and IgG2b, respectively. The PC-binding proteins possessed a typical phospholipase A2 activity, which was maximal at pH 9.5, depended on Ca++, and was specific for cleavage of fatty acid from the sn-2 position of phosphatidylcholine. The binding of aggregated IgG2b to the PC-binding proteins caused the ninefold increase in noted enzymatic activity in the presence of, but not in the absence of, Ca++ (5mM). The IgG-binding proteins on the other hand, lacked any detectable phospholipase A2 activity. Thus, the biochemical and biological properties of the PC- and IgG-binding proteins isolated from murine peritoneal macrophages are essentially identical to those homologous proteins previously isolated from P388D1 cells [20].
Androgen-Binding Protein↗
Effect of muramyl dipeptide analog on Salmonella enteritidis infection in beige mice with Chediak-Higashi syndrome.
Beige mutant (bg/bg) mice with Chediak-Higashi syndrome (CHS) were much more sensitive to virulent Salmonella enteritidis No. 11 strain than parental C57 BL/6 (+/+) or heterozygous (bg/+) mice, and they had weaker bactericidal activity against the organisms. Muramyl dipeptide (MDP) and N alpha-(N-acetyl-muramyl-L-alanyl-D-isoglutamyl)-N epsilon-stearoyl-L-lysine [MDP-Lys(L18)], a synthetic derivative of MDP, failed to confer any protection against the infection, but the MDPs showed some ability to stimulate the bactericidal activity in the peritoneal cavities and spleens of these mice. The bactericidal effect of MDP-Lys(L18) was dose-dependent, and the greatest effect was seen when it had been injected 24 hr before the infection. Multiple injections of MDP were much more beneficial than a single injection. Previous injection of N2,O2'-dibutyryl guanosine 3' : 5'-cyclic monophosphate (DB-cGMP) improved the impaired bactericidal capacity in beige mice, but the simultaneous injection of N6,O2-dibutyryl adenosine 3' : 5'-cyclic monophosphate (DB-cAMP) with DB-cGMP abolished the effect of DB-cGMP. The augmentation of bactericidal capacity by MDP-Lys(L18) was not affected by the injection of either DB-cGMP or DB-cAMP, suggesting that the effect of the MDPs was not related directly to cyclic nucleotide regulation in beige mice.
Acetylmuramyl-Alanyl-Isoglutamine↗
Augmentation of protective and antibacterial activity induced by muramyl dipeptides in CBA/N defective mice with X-linked immunodeficiency for Salmonella enteritidis infection.
Stimulation of resistance induced by muramyl dipeptide (MDP) and its analog, N alpha-MDP-N epsilon-stearoyl-L-lysine [MDP-Lys(L18)], was examined in experimental salmonellosis in CBA/N defective mice with X-linked immunodeficiency to virulent Salmonella enteritidis no. 11. An injection of either MDP or MDP-Lys(L18) did not induce any effective protection, but repeated injections of MDP-Lys(L18) (100 micrograms per mouse per day for 3 days consecutively) to the mice before bacterial challenge gave some protection. Multiple injections with MDPs once a day for several days consecutively strongly increased bactericidal capacity in the peritoneal cavities and spleens of the mice. Moreover, previous injection of the MDPs could elevate the phagocytic function of the reticuloendothelial system in the defective mice. These results indicate that nonspecific resistance of CBA/N defective mice to salmonella infection can be improved by previous administrations of MDPs.
Acetylmuramyl-Alanyl-Isoglutamine↗
Delayed hypersensitivity in murine salmonellosis: specificity of footpad reaction in mice infected with rough mutants of Salmonella typhimurium.
Delayed type (footpad) hypersensitivity (DTH) in BALB/c mice immunized with rough mutant strains of Salmonella typhimurium LT2 was examined. Injection of live organisms of an Rb mutant TV148 strain induced DTH in mice, while injection of the heat-killed organisms did not. The mice immunized with live organisms of the Ra, Rb, Rc, Rd, and Re mutant strains showed positive footpad reactions to the heat-killed cell antigen of LT2 (wild type) strain. The mice immunized with the Rb mutant strain also showed positive footpad swellings in response to heat-killed cell antigens of S. paratyphi A, S. paratyphi B, S. typhi, S. enteritidis, and S. cholerae-suis. Furthermore, positive reactions to antigens of Escherichia coli and Shigella flexneri were seen in the TV148-immunized mice, but the mice did not respond to heat-killed organisms of Pseudomonas aeruginosa or Staphylococcus aureus. The cross-reactive footpad reaction to E. coli could be transferred adoptively with T cells prepared from the spleens of TV148-immunized mice into syngeneic recipients. These results suggest that the cross-reactive DTH antigen(s) is widely distributed among related organisms such as Shigella and Escherichia.
Animals↗
Suppression of lipopolysaccharide-induced polyclonal B cell activation of murine spleen with heat-aggregated murine immunoglobulin G.
The effect of heat-aggregated immunoglobulin G's (HAgg-IgGs) on bacterial lipopolysaccharide- (LPS) induced polyclonal B cell activation (PBA) was studied. HAgg-IgGs (10 micrograms/ml or more) that were added to cultures of spleen cells obtained from BALB/c mice remarkably decreased the numbers of anti-trinitrophenyl (TNP) antibody-producing cells (APC) generated by LPS in cultures. This suppressive effect was seen when HAgg-IgGs were added within 1 hr after the initiation of culture. Later addition of HAgg-IgGs did not cause any effective suppression of the generation of APC. Moreover, the spleen cells, which had been pretreated with HAgg-IgGs, washed for removal of free HAgg-IgGs, and subsequently cultured, responded poorly to LPS. HAgg-IgG2b was more effective than HAgg-IgGs, but HAgg-IgG2a did not have any suppressive effect. A similar suppressive effect was observed when HAgg-IgG2b-Fc was added into culture, whereas none was noted with IgG2b-Fab. Indomethacin (IM), known as cyclooxygenase inhibitor, could completely abrogate the suppressive effects of HAgg-IgGs on LPS-induced PBA responses when it was added to the cell cultures together with HAgg-IgGs or to the cultures of HAgg-IgGs-pretreated cells. Addition of prostaglandin E2 (PGE2) showed strong suppression of the PBA responses of spleen cell cultures that had been pretreated with HAgg-IgGs and IM, but other PG analogues showed no suppression. Thus, it would appear that PGE2 has some role in the suppression of the LPS-induced PBA response.
Animals↗