Possible pathogenic effect of Streptococcus mitis superantigen on oral epithelial cells.
Explore the source record for details and available documents.
Antibodies, Monoclonal↗
Biomedical subjects
H Takada
Publications and source records attributed to H Takada.
Failure of treatment with interleukin-2 receptor-specific monoclonal antibody in acute coxsackievirus B3 myocarditis in mice.
T cell activation is assumed to play a crucial role in many viral infections. An important marker for the activation of T cells is the interleukin-2 receptor (IL-2R); resting T lymphocytes do not bear detectable amounts of IL-2R. AMT13, a rat monoclonal antibody against mouse IL-2R, inhibits interleukin-2-dependent cell growth both in vitro and in vivo. Therefore, to clarify the effects of anti-IL-2R antibody treatment upon coxsackievirus B3 (CB3)-infected C3H/He mice, AMT13, 1 microg/mouse per day, was administered, subcutaneously, starting on day 0 (group 2) in experiment I or on day 7 (group 4) in Experiment II for 7 days, respectively. Groups 1 and 3 were examined as infected controls. In both experiments, there was no significant difference in mortality or in the severity of myocarditis between the treated and the untreated groups. Also, myocardial CB3 titers on day 7 did not differ significantly between groups 1 and 2. In addition, the distribution of activated T cell subsets in the inflamed myocardium was not changed by the treatment, and the paucity of myocardial IL-2R-positive cells was confirmed in all groups. Effects of the antibody treatment were confirmed by a decrease in delayed type hypersensitivity. Although some reports have shown that anti-IL-2R antibody has been successfully applied to ameliorate acute renal graft-versus-host disease, to enhance survival of skin allografts, and to suppress diabetic insulitis, it did not exert a beneficial effect on acute CB3 myocarditis in mice.
Animals↗
Effects of levamisole, an immunomodulator, upon murine encephalomyocarditis virus myocarditis.
To test the therapeutic efficacy of levamisole, 5-week-old DBA/2 mice were inoculated intraperitoneally with 10 plaque-forming units of encephalo-myocarditis virus. Levamisole (2.5 mg/kg/per day) was administered intraperitoneally daily, starting simultaneously with the virus inoculation, in experiment I for 14 days, and daily on days 14 to 28 in experiment II in mice that survived to 14 days after virus inoculation. In experiment I, survival was higher, the severity of myocarditis was less, and myocardial virus titers were lower in treated than in untreated animals. In experiment II, levamisole was not effective. No significant changes in serum neutralizing antibody titers occurred in either experiment. Furthermore, levamisole prevented associated lymphoid organ atrophy induced by the virus infection. An additional in vitro study revealed the absence of anti-viral activity of the drug. Thus, levamisole may have favorable effects upon encephalomyocarditis virus myocarditis by preventing the virus-induced lymphoid organ atrophy and reducing myocardial virus replication in the acute stage.
Adjuvants, Immunologic↗
Contrasting effects of lipopolysaccharides (endotoxins) from oral black-pigmented bacteria and Enterobacteriaceae on platelets, a major source of serotonin, and on histamine-forming enzyme in mice.
By measurement of serotonin levels, the translocation of platelets to various tissues was examined following intravenous injection of a lipopolysaccharide (LPS) into C3H/HeN mice. There was a rapid platelet accumulation (within 5 min and particularly in the lung), followed by a slower accumulation in the liver, which reached its plateau 3-5 h later. The severity of the anaphylactoid shock corresponded well with the magnitude of the rapid response. LPSs from the oral black-pigmented bacteria, Porphyromonas gingivalis and Prevotella intermedia, were much more potent in inducing the rapid platelet response than were those from the Enterobacteriaceae Escherichia coli and Salmonella typhimurium. However, LPSs from these Enterobacteriaceae were significantly more potent than those from black-pigmented bacteria in inducing the slow platelet response. There was also a contrast between their abilities to induce histidine decarboxylase, which forms histamine from histidine: LPSs from the Enterobacteriaceae were much more potent than those from black-pigmented bacteria.
Acetylmuramyl-Alanyl-Isoglutamine↗
Structural feature of the major but not cytokine-inducing molecular species of lipoteichoic acid.
Previously, lipoteichoic acid (LTA) of Enterococcus hirae was found to exhibit definite cytokine-inducing activity but synthetic specimens which share the fundamental structural principles proposed for LTA had no corresponding activity. We also showed recently that several minor components totally less than 5% of the LTA fraction from E. hirae ATCC 9790 possessed the activity, whereas the major component (over 90%) did not [Suda, Y., Tochio, H., Kawano, K., Takada, H., Yoshida, T., Kotani, S., and Kusumoto, S. (1995) FEMS Immun. Med. Microbiol. 12, 97-112]. In the present study, the structure of the major component of LTA was studied in an attempt to elucidate the reason for the lack of the activity in the synthetic compounds. The major component of the LTA was first digested by hydrofluoric acid hydrolysis to cleave phosphodiester linkages present. The hydrolysis products were separated and characterized by means of NMR and MS. The linkage positions of the original phosphodiesters were determined from the NMR spectra of an alkali-treated product without hydrofluoric acid degradation. The compound was proved to consist of 1,3-linked poly(glycerophosphate) and a lipid anchor, Glc(alpha1-2)Glc(alpha1-3)acyl(2)Gro, the former being linked to the 6-position of the distal glucose of the latter. The 2-position of the glycerol residues in the glycerophosphate part were substituted by oligoglucose esterified partially with alanine. The gross structure elucidated here thus coincides with the previous conclusion described by Fischer [Fischer, W. (1990) in Glycolipids, Phosphoglycolipids and Sulfoglycolipids (Kates, M., ed.) pp. 123 234, Plenum Press, New York]. Thus, the molecular species with this so-called "LTA structure" is not responsible for the cytokine-inducing activity.
Alkaline Phosphatase↗
Extensive vesiculobullous eruption following limited ruby laser treatment for incontinentia pigmenti: a case report.
A 3-year-old girl with incontinentia pigmenti was referred for treatment of pigmented whorled macules on the trunk and limbs. Initially ruby laser therapy was only given to the legs. Wound healing was delayed. Two months later the patient developed extensive vesicles and erosions restricted to pigmented macules in both treated and untreated areas. Conservative treatment, including 2 weeks hospitalization, improved acute inflammation, but the remaining pigmentation was darker than originally seen. The apparent reappearance of an early cutaneous manifestation of this syndrome, seemingly triggered by laser therapy, would suggest such treatment is contraindicated.
Biopsy, Needle↗
Neonatal alloimmune thrombocytopenia associated with anti-human platelet antigen-3a antibody.
A sister and brother with neonatal alloimmune thrombocytopenic purpura (NAITP) caused by maternal anti-human platelet antigen (HPA)-3a are reported. The children had transient severe thrombocytopenia in the newborn period, and were treated with intravenous gamma-globulin and platelet concentrates from random donors. Although the sister had intracranial hemorrhage on day 2 postnatally, the development of the child has been normal and no neurological sequelae have been observed. The brother only had bloody stool when the platelet count was low, and did not have severe hemorrhagic manifestations. The diagnosis of NAITP was made by the sera from the mother, which contained anti-HPA-3a antibody directed against platelets of the children. The rate of recurrence might be high in this family, because the father of the patients was found to be homozygous for the HPA-3a gene.
Antigens, Human Platelet↗
Micrococcus luteus cells and cell walls induce anaphylactoid reactions accompanied by early death and serum cytokines in mice primed with muramyl dipeptide.
Micrococcus luteus strains at a dose of 500 microg of whole cells caused anaphylactoid reactions leading to death in some instances within 1 h in C3H/HeN mice primed with muramyl dipeptide (MDP, 100 microg). Tumor necrosis factor (TNF) and interleukin-6 (IL-6) were induced in the serum of half and of all the surviving mice, respectively. Cell wall specimens of M. luteus so far examined also caused anaphylactoid reactions accompanied by early death and one strain induced high levels of TNF and IL-6. Cytoplasmic membranes also induced IL-6. Essentially similar results were obtained with representative M. luteus cells and a cell wall specimen in MDP-primed C3H/HeJ mice. These results indicate that M. luteus has virulence activities that are associated with the induction of septic shock and systemic inflammatory diseases.
Acetylmuramyl-Alanyl-Isoglutamine↗
A novel component different from endotoxin extracted from Prevotella intermedia ATCC 25611 activates lymphoid cells from C3H/HeJ mice and gingival fibroblasts from humans.
A novel immunobiologically active fraction was prepared from a phenol-water extract of Prevotella intermedia ATCC 25611 by Sephadex G-100 column chromatography. The fraction consisted mainly of carbohydrate and protein and was devoid of fatty acid. The fraction showed high-molecular-weight bands (10,000 to 12,000) on deoxycholate polyacrylamide gel electrophoresis (DOC-PAGE) and was scarcely active in a Limulus test. We designated the fraction Prevotella glycoprotein (PGP). The PGP fraction showed strong mitogenicity on splenocytes and cytokine-inducing activities on peritoneal macrophages from both C3H/HeJ and C3H/HeN mice, and it stimulated human gingival fibroblasts to produce cytokines. The activities of the PGP fraction were resistant to heat inactivation (100 degrees C for 1 h) and protease treatments and were scarcely inhibited by polymyxin B. In contrast, the purified lipopolysaccharide fraction (LPS-PCP) extracted from the same bacterium with a phenol-chloroform-petroleum ether mixture, which showed strong Limulus activity and a single low-molecular-weight band (approximately 3,000) on DOC-PAGE, lacked the activities on splenocytes and macrophages from C3H/HeJ mice and human gingival fibroblasts. The activities of the LPS-PCP fraction on cells from C3H/HeN mice were completely inhibited by polymyxin B. The LPS extracted from the same bacterium with hot phenol-water (LPS-PW) exhibited the properties of both the PGP fraction and the LPS-PCP fraction. These findings suggest that the unique bioactivities of the LPS-PW fraction of oral black-pigmented bacteria reported to date, which differed from those of the classical endotoxin, were derived from the PGP fraction and not from the LPS itself.
Adjuvants, Immunologic↗
Theiler's murine encephalomyelitis virus subgroup strain-specific infection in a murine macrophage-like cell line.
We compared infection of a murine macrophage-like cell line, J774-1, with two Theiler's murine encephalomyelitis virus subgroup strains. The GDVII strain, which is highly virulent and produces acute polioencephalomyelitis in mice, did not actively replicate in J774-1 cells, although there was a significant inhibition in cellular protein synthesis. In contrast, the DA strain, which is less virulent and causes demyelination with a persistent virus infection, productively infected J774-1 cells; however, there was less virus produced than in BHK-21 cells, and there was little if any cellular protein shutoff. These in vitro data may provide some explanation for the biological activities that are observed between both subgroup strains.
Actins↗
Captopril suppresses interstitial fibrin deposition in coxsackievirus B3 myocarditis.
The effects of captopril on murine coxsackievirus B3 (CB3) myocarditis were investigated, with focus on interstitial fibrin deposition and changes in the connective tissue matrix. Captopril was administered intraperitoneally at a dose of 0.1 mg/g to CB3-infected mice daily on days 10-30 in experiment I (inflammatory phase) and on days 30-60 in experiment II (fibrotic phase). In experiment I, mouse survival was higher in the captopril-treated group than in the untreated group. Histological improvement, including prevention of extravasated fibrin deposition, maintenance of connective tissue architecture, suppression of myocyte hypertrophy, and prevention of myosin isoform shift from alpha to beta, was observed in captopril-treated mice in experiment I, but not in experiment II; in experiment II, captopril administration suppressed thickening of the interstitial reticulin fibers. Captopril inhibited inflammatory fibrin deposition, postmyocarditic myocyte hypertrophy, and ventricular remodeling during the inflammatory phase, but not during the fibrotic phase, of CB3 myocarditis in mice.
Animals↗
Comparison of bactericidal effects of commonly used antiseptics against pathogens causing nosocomial infections. Part 2.
Opportunistic infections caused by gram-negative rods (GNR), conventionally regarded as organisms with low or no pathogenicity, and intractable infections caused by various resistant organisms pose a great problem now. In view of this, we determined the bactericidal effects of 5 commonly used disinfectants using as the test strains Xanthomonas maltophilia and Serratia marcescens, chosen among other GNR since they often cause nosocomial infections. Regarding the bactericidal activities against X. maltophilia and S. marcescens, both sensitive strains and resistant strains were killed within 20 s of exposure to povidone-iodine and sodium hypochlorite. With chlorhexidine, 1 strain each of both species was not killed within 10 min of exposure at a concentration of 0.2%. Both sensitive strains and resistant strains of X. maltophilia were killed within 20 s of exposure to benzalkonium at 0.02%, while a concentration of 0.1% was required for benzalkonium to kill S. marcescens within 20 s. With Tego-51, both sensitive strains and resistant strains of X. maltophilia were killed within 20 s at 0.02%, while 1 strain of S. marcescens was not killed within 20 s at a concentration of 0.1%. In the use of disinfectants, comparative bactericidal effects of various disinfectants against clinical isolates should be taken into consideration.
Anti-Infective Agents, Local↗
The influence of long-term treatment with povidone-iodine on thyroid function.
Povidone-iodine (PVP-I) is generally very safe, but cases of thyroid dysfunction induced by PVP-I have been reported. The effect of long-term treatment with PVP-I on thyroid function was to be assessed. In 40 inpatients of the department of neurology, the status of the use of PVP-I preparations and their effects on serum inorganic iodine levels and thyroid functions were investigated. In 27 patients treated with PVP-I for a long term, inorganic iodine levels were significantly increased as compared to those in 13 patients without PVP-I treatment. Out of 27 patients treated with PVP-I in the long term, subclinical hypothroidism was seen in 3 patients, mild hyperthroidism was seen in 1 patient, and subclinical hyperthyroidism was suspected in 7 patients. Patients treated with PVP-I for a long time should be observed carefully for any manifestation of thyroid dysfunction.
Amyotrophic Lateral Sclerosis↗
Individual variation of acetohexamide reductase activities in liver microsomes and cytosol of rats.
We examined individual variations in acetohexamide reductase activities in liver microsomes and cytosol of rats. Large differences among individuals were observed for acetohexamide reductase activity in liver microsomes of male Fischer-344 (Fischer), Sprague-Dawley (SD) and Wistar rats at 9 weeks of age, except in the Wistar-Imamichi (Wistar-IM) strain. These four strains of female rats did not exhibit any microsomal enzyme activity. Although acetohexamide reductase activities were fully detectable in liver cytosols from all the strains of male and female rats, there was neither strain-related difference nor considerable individual variation in the cytosolic enzyme activity. In liver microsomes of male Fischer rats at 4 weeks of age, acetohexamide reductase activity was not detectable. The microsomal enzyme activity in male Fischer rats markedly increased at 6 weeks of age to approach the levels at 9 and 12 weeks of age, with large individual variations.
Aging↗
Influence of exercise on QT dispersion in ischemic heart disease.
UNLABELLED: QT dispersion (QTd: maximum QT interval-minimum QT interval) is associated with severe cardiac arrhythmia and with abnormal ventricular repolarization. We investigated the influence of exercise on QTd in patients with ischemic heart disease. On standard 12-lead electrocardiograms, QTd was measured before and after treadmill exercise in 7 normal subjects, 17 patients with effort angina pectoris (and > or = 75% stenosis on coronary arteriography), and 33 patients with old myocardial infarction. Bazett's formula was used to obtain the corrected QTd (QTcd). The pre-exercise resting QTcd was 45.9 +/- 10.6, 44.3 +/- 15.2, and 74.8 +/- 28.1 msec in the respective groups, being significantly greater in the infarct group (p < 0.05). The QTcd at 5 min after exercise was respectively 49.3 +/- 9.0, 58.8 +/- 19.9, and 75.4 +/- 30.9 msec (p = 0.0347, infarct vs. controls). The difference in QTcd was significant for the angina group before and after physical exercise (p = 0.0003). There was a significant increase of QTcd after exercise in the angina group whether or not the patients were receiving beta-blockers. The infarct patients without beta-blocker therapy showed an increase of QTcd after exercise, while those receiving beta-blockers showed a decrease. The post-exercise difference between these subgroups was significant (p = 0.0351). CONCLUSIONS: QTcd was significantly increased by exercise in the angina group, possibly reflecting impaired repolarization due to ischemia. Inhibition of the increase in QTd by beta-blockers suggested a possible preventive effect on severe arrhythmias due to nonhomogeneous ventricular repolarization.
Adrenergic beta-Antagonists↗
Nitric oxide and murine coxsackievirus B3 myocarditis: aggravation of myocarditis by inhibition of nitric oxide synthase.
OBJECTIVES: This study sought to investigate the effects of nitric oxide inhibition in a murine model of coxsackievirus B3 myocarditis. BACKGROUND: Little is known about the contribution of nitric oxide to the pathophysiology of myocarditis. METHODS: Antiviral activity was tested in vitro using nitric oxide inhibition by treatment with activated macrophages of NG-nitro-L-arginine methyl ester. In the in vivo experiments, NG-nitro-L-arginine methyl ester and NG-nitro-D-arginine methyl ester (both at 100 micrograms/ml) were administered to C3H/He mice early (days 0 to 14) and late (days 14 to 35) after infection with coxsackievirus B3. RESULTS: In the in vitro experiments with interferon-gamma- and lipopolysaccharide-induced activated murine macrophages, treatment with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester, but not its inactive enantiomer NG-nitro-D-arginine methyl ester, restored coxsackievirus B3 titers. In the in vivo experiments in the early treatment group, myocardial virus titers were higher in NG-nitro-L-arginine methyl ester-treated than infected untreated animals, and both inflammatory cell infiltration and necrosis were more severe. In the late treatment group, more severe necrosis and more dense myocardial and perivascular fibrosis were observed in NG-nitro-L-arginine methyl ester-treated than in infected untreated animals. NG-Nitro-D-arginine methyl ester administration was ineffective. CONCLUSIONS: Nitric oxide inhibition increases myocardial virus titers, resulting in the aggravation of cardiac pathology in the early stage of coxsackievirus B3 myocarditis. In the late stage, it induces more severe cardiomyopathic lesions. Nitric oxide plays a defensive role in the pathogenesis of coxsackievirus B3 myocarditis.
Animals↗
Assessment of posterior aortic wall motion using echocardiogram in patients with atrial fibrillation.
BACKGROUND AND HYPOTHESIS: Noninvasive evaluation of left ventricular (LV) diastolic function was performed on 12 patients with atrial fibrillation (AF) using posterior aortic wall echocardiogram and a parameter for determining the optimal heart rate in patients with chronic atrial fibrillation was considered. METHODS: Subjects were divided into two groups; one with no underlying cardiac disease (AF only group; n = 7) and the other with dilated cardiomyopathy (DCM group; n = 5). Left atrial emptying index (LAEI) obtained from the posterior aortic wall echocardiogram was used as the parameter of LV diastolic function, and R-R interval-LAEI relation and minimum R-R interval showing LAEI = 1.0 were investigated and compared between the two groups. RESULTS: There was a good correlation between R-R interval and LAEI until LAEI of 1.0 was obtained in all patients. Slope of the regression line was significantly steeper in the AF only group than in the DCM group, and minimum R-R interval showing LAEI = 1.0 was significantly shorter in the AF only group. CONCLUSION: Assessment of R-R interval-LAEI relation was useful for the noninvasive evaluation of LV diastolic function, and this parameter could be used for clinical application to determine the optimal heart rate in atrial fibrillation.
Aorta↗
Lipopolysaccharides from Porphyromonas gingivalis, Prevotella intermedia and Actinobacillus actinomycetemcomitans promote osteoclastic differentiation in vitro.
Bacterial lipopolysaccharides possess bone-resorbing activity. Here, lipopolysaccharides from three putative periodontopathic bacteria were examined for effects on osteoclast-like cell formation of bone marrow cells from lipopolysaccharide-responsive C3H-HeN and non-responsive C3H/HeJ mice. The bone marrow cells were cultured with or without various doses of lipopolysaccharide in the presence of 1,25-dihydroxyvitamin D3 and dexamethasone. These lipopolysaccharide preparations significantly increased the number of osteoclast-like cells formed in the culture of C3H/HeN marrow cells; the same as lipopolysaccharides from Escherichia coli and a synthetic lipid A with E. coli-type structure (LA-15-PP), at doses from 0.1 to 1 microgram/ml. This stimulating effect of each lipopolysaccharides was uniformly abrogated by the addition of polymyxin B at 5 micrograms/ml. All the lipopolysaccharide and the synthetic lipid A had no effect on osteoclast formation of the C3H/HeJ marrow cells, whereas lipopolysaccharide from Porphyromonas gingivalis and Prevotella intermedia showed significant mitogenic activity on C3H/HeJ spleen cells. It seems likely that the activity of lipopolysaccharides to augment osteoclast-like cell formation in the bone marrow cell cultures is derived from a common structure of the lipid A portion.
Acid Phosphatase↗