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Biomedical subjects

F Matsuda

Publications and source records attributed to F Matsuda.

At least 109 records · Page 6Linked to original sources
PubMed1982

Mode of action of staphylococcal leukocidin: effects of the S and F components on the activities of membrane-associated enzymes of rabbit polymorphonuclear leukocytes.

The cytotoxic action of the S component of leukocidin from Staphylococcus aureus on rabbit polymorphonuclear leukocytes was supported by the following observations, (i) Leukocytes displayed a large chemotactic response to the S component (10(-10) M) as well as to the chemotactic factor N-formylmethionylleucylphenylalanine (10(-11) M). (ii) The S component stimulated high levels of phospholipase A2 activity in the cell membranes, with concomitant synthesis and release of prostaglandins. (iii) Uptake of 45Ca into leukocytes exposed to the S component was about double the rate of uptake into untreated cells. The increased 45Ca uptake into the cells was not inhibited by trifluoperazine and ruthenium red. (iv) Indomethacin and alloxazine, which had no effects on the binding of the S component to the cells, attenuated markedly the stimulation of phospholipase A2 activity, the syntheses of prostaglandins, and the increased uptake of 45Ca caused by the S component. The F component of leukocidin, bound to rabbit leukocytes with the aid of the S component, rapidly induced complete release of 86Rb from preloaded leukocytes. This release resulted from stimulation of ouabain-insensitive (Na+ + K+)-adenosine triphosphatase activity and inhibition of cyclic AMP-dependent protein kinase.

Animals↗
PubMed1981

Mode of action of staphylococcal leukocidin: relationship between binding of 125I-labeled S and F components of leukocidin to rabbit polymorphonuclear leukocytes and leukocidin activity.

The binding of (125)I-labeled S component to rabbit polymorphonuclear leukocytes was found to be concentration dependent and saturable at 37 degrees C. Scatchard analysis of the binding curve gave a straight line, indicating that S component binds to a single population of sites. The dissociation constant, K(D), derived from the Scatchard plot was 5.57 x 10(-9) M, and the number of binding sites per leukocyte was calculated to be approximately 5,300. Unlabeled S component (10(-8) M) or subunit B of cholera toxin (10(-7) M) readily competed with (125)I-labeled S component binding, and the labeled S component, preincubated with ganglioside G(M1) at equimolar proportions for 5 min, lost the binding capacity to the leukocyte membranes. The binding number of (125)I-labeled F component to leukocidin-sensitive cells, such as rabbit polymorphonuclear leukocytes and the established human myelocytic leukemia cells, in the absence and in the presence of the unlabeled S component (2.1 nM), was calculated to be 50 and 1,300 molecules per cell, respectively. This increased binding of the labeled F component was time and temperature dependent. The binding number of labeled F component to other cell types comparatively insensitive to leukocidin, such as erythrocytes, adipocytes, intestinal cells, and HeLa cells, was calculated to be less than 50 molecules per cell in spite of the sufficient amount of unlabeled S component bound to their cells. These observations are consistent with the view that in rabbit leukocyte the S component, preferentially bound to the cell surface at 5,300 molecules per cell, contributes to enhance the F component binding up to about 1,300 molecules per cell and may thus play a role of synergistic action of both leukocidin components on the cell membranes in the leukocytolysis.

Adipose Tissue↗
PubMed1980

Crystallization and properties of staphylococcal leukocidin.

Two components (F and S) of leukocidin were isolated and purified from broth culture of V8 strain of Staphylococcus aureus. There was loss of leukocidin activity during the separation, which was regained by mixing the components. Each component was apparently homogeneous by several criteria. The F and S components were crystallized (by salting out with saturated (NH4)2SO4 at pH 7.0) in the form of square plates and very fine needles, respectively, and the molecular weights of the components were approx. 32 000 and 31 000, respectively. The isoelectric points of the F and S components were pH 9.08 and 9.39, respectively. No detectable half-cystine and free sulfhydryl groups were found in either component. Amino-terminal amino acid analysis of both components showed a single alanine residue. The F and S components of leukocidin acted synergistically on granulocytes from rabbit peripheral blood and a minimum lethal dose of 0.5 ng of each component destroyed all granulocytes at a concentration of 10(6) cells/20 microliter.

Amino Acids↗
PubMed1980

Fixation and inactivation of staphylococcal leukocidin by phosphatidylcholine and ganglioside GM1 in rabbit polymorphonuclear leukocytes.

Staphylococcal leukocidin is resolved by chromatography on carboxymethyl cellulose columns into two components, which are designated F (fast) and S (slow). Fixation and inactivation of both components were studied as follows. (i) Leukocidin activity was confined to the first 10 min of intoxication, and the maximal effect resulted from treating 10(6) rabbit peripheral polymorphonuclear leukocytes per 20 mul with 0.5 ng of each component of leukocidin. The S component was more responsible for the interaction with the leukocytes than the F component. (ii) The F component was inactivated by phosphatidylcholine at concentrations which corresponded to molar proportions of 1:1 and bound to [(14)C]phosphatidylcholine at equimolar proportions. (iii) The S component was inactivated by ganglioside G(M1) at 1:1 molar proportions, but not by any of the related glycolipids. Ganglioside G(M1) also was precipitated with the S component by a gel diffusion technique. Subunit B of cholera toxin competitively inhibited the binding of the S component to rabbit leukocyte membranes. This indicates that ganglioside G(M1) may resemble or be part of the receptor site for the S component.

Animals↗
PubMed1977

Effects of halothane on coronary and systemic circulations, myocardial metabolism and blood flow distribution within the canine heart.

Myocardial metabolism, blood flow distribution within the heart, and coronary and systemic circulations were observed during halothane anesthesia using 15 mongrel dogs. Pao2 and Paco2 were maintained near 100 and 40 torr respectively throughout the study. As arterial halothane content increased, most parameters of systemic circulation were depressed significantly. Coronary blood flow was reduced in parallel with myocardial oxygen consumption (MVo2) (r=+0.89, pless than0.001). Myocardial contractility decreased significantly as anesthesia deepened. MVo2 and myocardial CO2 production were reduced as arterial halothane concentration rose. Arterial-coronary venous difference in blood oxygen content remained unchanged even in deep stage. Lactate and pyruvate were continuously taken up by the myocardium, although the amounts of uptake were reduced as anesthesia progressed. Calculated excess lactate and redox potential did not show any signs of myocardial hypoxia even in deep halothane anesthesia. Among major hemodynamic parameters, left ventricular dp/dt max showed the closest correlation with MVo2. Microsphere injection method was used to observe blood flow distribution within the heart. Halothane did not influence the distribution significantly and I/O ratio of the left ventricular free wall remained near 1.0 during the study.

Animals↗
PubMed1974

Pleiotropic alteration of activities of several toxins and enzymes in mutants of Staphylococcus aureus.

Pleiotropic alteration of several genetic characters including toxin production was quantitatively shown with a strain of Staphylococcus aureus of phage type 80, 81 which had been given a very specific genetic marker (temperature sensitivity of mannitol fermentation) to avoid confusion by contamination. Thus, alpha-hemolysin hyperproducers obtained by N-methyl-N'-nitro-N-nitrosoguanidine (NTG) mutagenesis were very often hyperproducers of DNase, coagulase, and protease. Their colonies were less yellow than the parent. DNase hyperproducers obtained after NTG mutagenesis were also often hyperproducers of alpha-hemolysin, coagulase, and protease, with colonies less yellow than the parent. Almost all of the revertants obtained by mutagenesis with ethyl methane sulfonate with respect to alpha-hemolysin or DNase were shown to have simultaneously become hypoproducers of alpha-hemolysin, DNase, and protease. Since the pleiotropic alteration of multiple functions was thus quantitatively confirmed, the mechanism underlying this phenomenon should probably be related to a regulatory mechanism common to them.

Alkanesulfonates↗