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E Storch

Publications and source records attributed to E Storch.

35 records · Page 2Linked to original sources
PubMed1985

Attempts to correlate interferon induction and activation of natural killer cells by Corynebacterium parvum.

Intraperitoneal (i.p.) injection of Poly I:Poly C resulted in high interferon titers in the peritoneal wash fluid and in the serum of mice, which was maximal at 4 to 6 h after injection. In contrast, no interferon could be measured in the peritoneal fluid at various times after injection of C. parvum. Also, all attempts to induce serum interferon by C. parvum were unsuccessful. However, both Poly I:Poly C and C. parvum were causing the activation of Natural Killer (NK) cells in the cell population recovered from the peritoneal cavity. From adoptive transfer experiments, there was no indication that C. parvum induced a soluble mediator causing the activation of NK cells. There was also no indication that the interferon activity in the peritoneal cavity of C. parvum-treated mice might have been masked by the presence of an inhibitory molecule interfering with the antiviral effect of interferon in the assay. Our data may suggest activation of NK cells by C. parvum to be independent of interferon induction. Accordingly, we have observed that the injection of anti-interferon did not abolish NK cell activation by C. parvum. Thus, there is the interesting possibility of an interferon-independent mechanism of NK cell activation. However, we have additionally shown that doses of murine alpha/beta interferon as low as 1 IU per mouse caused a significant activation of NK cells in the peritoneal cavity upon i.p. injection. Thus, interferon itself is extremely potent in activating NK cells.

Animals↗
PubMed1984

Induction of interferon gamma in mouse spleen cells by culture supernatants of mycoplasma arthritidis.

Factor(s) in the supernatant of cultured mycoplasma arthritidis (MAS) represented potent inducers of interferon (IFN) in cultures of mouse spleen cells. Responding mouse strains included A/J, BALB/c, CBA, C3H, and DBA/2 whereas spleen cells of C57BL/6 and C57BL/10 mice were nonresponders. Interferon production was controlled by the I region of the H-2 locus. Treatment of CBA spleen cells by anti-thy-1 antibody plus C abolished IFN production. A similar effect was seen when CBA spleen cells were freed of macrophages by passage through Sephadex G-10 columns. Pure macrophages themselves, however, were not producing IFN when treated by MAS. Macrophage-depleted CBA spleen cells could be reconstituted to produce IFN by the addition of 2-ME. Interferon induction by CBA spleen cells was independent of lymphoproliferation as evidenced by experiments utilizing mitomycin C. The IFN induced by MAS represented IFN gamma (gamma), since it was acid-labile and neutralized by a specific antiserum.

Animals↗
PubMed1984

[Time dependence of Ca supply in rat and rabbit myocardium].

The time dependence of Ca supply in rat (R) and rabbit myocardium (K) for the activation was analyzed by the action potential area up to 50% of repolarization (APA50) of the action potential (AP) during the electrical restitution as well as by extra contractions (EC) during the mechanical restitution and subsequent postextrastimulatory contraction (PEC) or potentiation (PEP) in isometrically contracting papillary muscle at different extracellular Ca concentrations (Cae). In K a considerable increase in APA50 of the EC-AP during the electrical restitution within the interval of rhythmical contraction (T) strongly correlates with the subsequent PEP. In R both the alteration of the APA50 and the PEP are smaller than in K. Compared with K in R the mechanical restitution is delayed, but accelerated by rising Cae as demonstrated by increasing EC/T. The course of mechanical restitution and the low PEP are regarded to be connected with the fact that the sarcoplasmic reticulum is the main source of activator Ca in R. Differences in both electrical and mechanical restitution and, especially the higher PEP, agree with the sarcolemma as the main source of activator Ca in K.

Action Potentials↗
PubMed1983

Herpes simplex virus type 1-induced interferon production and activation of natural killer cells in mice.

Cultures of peritoneal exudate cells (PEC) of non-immune C57BL/6 mice reacted to infectious herpes simplex virus type 1 (HSV), but not to non-infectious virions by producing interferon. Similarly, when the virus preparations were injected intraperitoneally (i.p.) and interferon was determined in the wash-out fluid, interferon could only be detected after injection of infectious HSV. All interferons were mixtures of interferon-alpha and -beta. The cell that produced interferon was not sensitive to anti-theta serum or anti-asialo-GM1 serum, it was retained on nylon wool columns and removed by plastic adherence. Silica treatment of PEC abolished HSV-induced interferon production whereas irradiation by 2000 R was without effect. Pure cultures of mouse T cells did not produce interferon when treated with infectious HSV whereas pure cultures of mouse bone marrow macrophages did produce interferon. Thus, we suggest that in PEC the cells which produced interferon were of the macrophage lineage. In further experiments we have analysed in vivo activation of natural killer (NK) cells in the peritoneal cavity of mice. Non-infectious virions were as effective as infectious HSV and doses of HSV too low to induce measurable titres of interferon caused a marked activation of NK cells.

Animals↗
PubMed1982

Interferons and bacterial infections.

Viruses have been established initially as interferon inducers and interferons have been considered to be antiviral proteins only. By our article we wish to draw attention to two observations: a) bacteria and derivatives thereof also are inducing the production of interferon b) interferons activate a number of defense mechanisms that are of potential relevance in antibacterial resistance. These two observations are not new. However, we believe, they deserve renewed attention within the framework of the pleiotropism of interferon effects and of the complexity of antibacterial defense mechanisms.

Animals↗
PubMed1982

Induction of interferon in murine bone marrow-derived macrophage cultures by 10-carboxymethyl-9-acridanone.

10-Carboxymethyl-9-acridanone (CMA) induced high titers of interferon (IFN) in murine leukocyte cultures. Thymocytes, lymph node, spleen and peritoneal exudate cells responded to CMA with IFN production. Pure macrophages derived from the bone marrow were the most efficient producers of CMA-induced IFN. The yields of IFN-alpha, beta in the macrophage supernatants depended on the concentration of the inducer and titers up to 3000 IU/ml were measured after exposure to the optimal dose (500 micrograms/ml). CMA was found to be the first low molecular weight compound that induced in vitro titers of IFN nearly as high as obtained after exposure to Newcastle disease virus, which is one of the most potent interferon inducers.

Acridines↗
PubMed1982

The influence of atherogenic diet on electromechanical coupling in rabbit myocardium.

To characterize the role of the SR in the electromechanical coupling process in rabbit myocardium after a 12-week-long atherogenic diet containing cholesterol and oil, the influence of changes in Ca2e+ on isometric force, relaxation rate, and resting potentiation of isolated trabeculae were compared with 45Ca2+ binding and uptake by the SR. The diet produces a more strongly expressed resting potentiation of force at 1.25 and 2.5 mM Ca2e+ and an increase in the Vmax equivalent, the contractility index [(dF/dt)max/F'] and the relaxation index [-(dF/dt)max/F]. A higher Ca2e+-accumulating activity of heart microsomes from animals was observed after the diet. It is concluded that changes of SR function are involved in the mechanism responsible for modification of electromechanical coupling induced by cholesterol- and oil-containing diet.

Animals↗
PubMed1982

[Diet induced changes of Ca-regulation in rabbit papillary muscle. 1. Contraction and relaxation following a cholesterol diet].

To characterize consequences of cholesterol induced increases of the Na content on the Ca regulation in rabbit myocardium the influence of increasing extracellular Ca (Cae) on isometric contraction and relaxation of papillary muscles has been investigated after a 12 weeks lasting cholesterol-rich diet. After cholesterol-rich diet increasing Cae caused a higher augmentation in peak tension T, accompanied by a decreased index in contractility [Formula: see text], an insignificantly prolonged time to peak tension TPT, and a decrease in the refractory period, which was extended compared with the control group. A delay in relaxation is demonstrated by the maximum relaxation rate [Formula: see text], the half time of relaxation RT 1/2 and more pronounced by a prolonged relaxation time RT. The results correspond with changes in the Na content published earlier and are in agreement with the assumption that a Na-Ca exchange is involved in beat-to-beat regulation in rabbit myocardium; thereby the cholesterol component of atherogenic diet promotes Ca enhancement in rabbit cardiac cells.

Animals↗
PubMed1982

[Diet-induced changes on Ca-regulation in rabbit papillary muscle. 2. Contraction, relaxation and rest potentialization following a rapeseed diet].

To characterize consequences of rape oil-induced changes on the Ca regulation in rabbit papillary muscle, the influence of increasing extracellular Ca (Cae) on contraction, relaxation and resting potentiation of tension has been investigated after a 12 weeks lasting rape oil-diet. After oil diet increasing Cae caused a similar augmentation in peak tension T accompanied by an increased index in contractility [Formula: see text], a significantly shortened time to peak tension and a decline in refractory period. A higher relaxation rate is demonstrated by the maximum relaxation rate [Formula: see text], the half time of relaxation RT 1/2 and relaxation time RT. The resting potentiation of the isometric contraction was enhanced. The results are in agreement with the assumption that the sarcoplasmic reticulum (SR) is more involved in Ca regulation after the oil diet than in the control group. This may be related to differences in the phospholipid content of SR membranes.

Animals↗
PubMed1980

[Modifications of electromechanical coupling in the rabbit myocardium following cholesterol-oil diet during changing Ca2+ supply].

To characterize the electromechanical coupling in rabbit myocardium after a 12 weeks lasting lipid-rich diet the influence of increasing extracellular Ca2+ on isometric contractions of isolated trabeculae has been investigated. Only after lipid-rich diet the Ca2+-induced augmentation in isometric tension was accompanied by an increase in a Vmax equivalent, in the index of contractility dk/dtmax divided by K', and in the relaxation index -dk/dtmax divided by K. The results correspond with changes in the sarcoplasmic reticulum function reflected in a higher Ca2+ accumulating ability of isolated microsomes.

Animals↗
PubMed1977

Therapeutic studies with BCG, cyclophosphamide and surgery alone and in combination on the autochthonous mammary carcinoma of the rat.

In a randomized study the effects of BCG, cyclophosphamide and surgery alone and in combination on the mammary carcinoma (induced by 7,12-dimethylbenz(a)anthracene) of the rat were investigated. Surgical excision of the tumours increased the survival time. Cyclophosphamide retarded growth of tumours and delayed the appearance of relapses compared to surgery. A single, intravenous injection of BCG (10(7) viable organisms) showed no statistically significant retardation of tumours. Immunotherapy with BCG could not increase the effectiveness of cyclophosphamide or surgery or their combination.

Animals↗
PubMedDate not supplied

Effects of hypoxia, simulated ischemia and reoxygenation on the contractile function of human atrial trabeculae.

Hypoxia, ischemia and reoxygenation cause contractile dysfunction which will be characterized by the time course of isometric contraction of human atrial trabeculae. Post-rest potentiation (PRP) and postextrastimulatory potentiation (PEP) were elicited to obtain indirect information about the the role of the sarcoplasmic reticulum (SR) in excitation-contraction coupling. As lipid peroxidation could cause SR dysfunction, thiobarbituric acid reactive substances (TBARS) were measured. After 30 min of hypoxia (H) or simulated ischemia (H combined with acidosis-SI), contractile force decreased to 15% and 6%, respectively, of control (p < or = 0.05), whereas the normalized rate of both contraction and relaxation increased. In group H, rapid reoxygenation produced a recovery of contractile force to about 60%. After post-hypoxic reoxygenation the TBARS concentration was increased. In group SI, rapid reoxygenation and a rather gradual correction of acidosis produced complete recovery of contractile force. PRP and PEP were maintained during H and SI. Particularly post-ischemic reoxygenation caused a marked depression of PRP and partly of PEP. Thus, alteration of SR Ca2+ handling occurs predominantly during reoxygenation rather than during H or SI, probably associated with the damaging effect of increased oxygen radicals. The depression of potentiation occurred along with delayed relaxation, temporary increased resting force, mechanical alternans, and spontaneous activity which are further characteristics for SR dysfunction. Thus, for a possibly beneficial effect of low pH during SI combined with its gradual correction during reoxygenation on the recovery of contractile function, developed force should not be the only index.

Action Potentials↗
PubMedDate not supplied

Protection by polyI:polyC against infection with herpes simplex virus in mice pretreated with Corynebacterium parvum.

The effect of Corynebacterium parvum on the protection by polyinosinic-polycytidylic acid (polyI:polyC) against lethal infection with Herpes simplex virus type 1 (HSV) was studied in mice. Pretreatment with C. parvum resulted in prolonged survival times in all experiments. One third of the mice survived an infection with 100 LD50, whereas all mice died when treated with polyI:polyC alone. Increased protection was observed up to 6 weeks after pretreatment and only seen when both C. parvum and polyI:polyC were given at the same site of injection (intraperitoneally). Protection against HSV correlated with increased interferon (IFN) activities induced by polyI:polyC in the peritoneal cavity of C. parvum-pretreated mice. In these mice, natural killer cell activity of peritoneal exudate cells (PEC) was also augmented in response to polyI:polyC. Protection was markedly decreased by intraperitoneal injection of silica or of an antiserum against murine IFN. It appears that increased local levels of IFN presumably produced by macrophages in response to polyI:polyC in C. parvum-pretreated mice play the major role in the antiviral defence in our model and that activation of NK cells may be a secondary effect of IFN.

Adjuvants, Immunologic↗