STUDIES ON THE EFFECTS OF PHAGOCYTIC STIMULATION ON MICROBIAL DISEASE: IV. THE INFLUENCE OF 1,4-DIMETHYL-7-ISOPROPYLAZULENE WITH AND WITHOUT DIHYDROSTREPTOMYCIN ON EXPERIMENTAL TUBERCULOSIS IN GUINEA PIGS

1955 ◽  
Vol 1 (8) ◽  
pp. 622-633
Author(s):  
László Kátó ◽  
Béla Gözsy
Keyword(s):  
Guinea Pigs ◽  
Defense Mechanism ◽  
Experimental Tuberculosis ◽  
Simultaneous Treatment ◽  
Appropriate Treatment ◽  
Parasite Relationship ◽  
Azulene Derivative ◽  
Tuberculosis Therapy ◽  
Host Parasite

The outcome of experimental tuberculosis in guinea pigs was favorably influenced by treatment with 1,4-dimethyl-7-isopropylazulene. This compound had no antituberculous properties in vitro, but stimulates phagocytic activity of cells of the reticulo-endothelial system. Effects of simultaneous treatment with the azulene derivative and dihydrostreptomycin on well-established tuberculosis were similarly studied. Therapeutical effect of dihydrostreptomycin was significantly increased by the simultaneous treatment with the azulene. This experiment brought evidence that the host–parasite relationship in experimental tuberculosis can be favorably influenced for the benefit of the host by appropriate treatment acting against the parasite and simultaneously stimulating the defense mechanism of the host. The authors discuss the need for more research in tuberculosis therapy directed toward finding ways of stimulating the cell-linked defense mechanism of the host against bacterial invaders.

STUDIES ON THE EFFECTS OF PHAGOCYTIC STIMULATION ON MICROBIAL DISEASE: V. STIMULATION OF PHAGOCYTIC ACTIVITY OF MONOCYTES AGAINST TUBERCLE BACILLI, STRAIN BCG

1956 ◽  
Vol 34 (1) ◽  
pp. 571-579
Author(s):  
Béla Gözsy ◽  
László Kátó
Keyword(s):  
Phagocytic Activity ◽  
Guinea Pigs ◽  
Saline Solution ◽  
Defense Mechanism ◽  
Direct Action ◽  
Intraperitoneal Administration ◽  
Cellular Defense ◽  
Appropriate Treatment ◽  
Stimulation Of

Monocytes were obtained by the washing of the peritoneal cavity of guinea pigs with Hanks' solution six days after intraperitoneal administration of a saline solution containing glycogen. Phagocytosis of tubercle bacilli (BCG strain) was studied after a one hour incubation at 37 °C. under the influence of histamine and 1,4-dimethyl-7-isopropyl-bicyclo-decapentane, which latter substance had shown a beneficial influence on the outcome of experimental tuberculosis. Histamine increased the phagocytic activity of monocytes, within the limits of 1 μgm. to 10 μgm per ml. This stimulation was inhibited in vitro by a synthetic antihistamine substance. Fifty and 100 μgm. per ml. histamine decreased the phagocytosis of tubercle bacilli (BCG) by the monocytes. Monocytes withdrawn from histamine treated guinea pigs showed no stimulated activity. From 0.5 to 100 μgm. per ml. of 1,4-dimethyl-7-isopropylbicyclo-decapentane stimulated the phagocytic activity of monocytes against tubercle bacilli (BCG) in vitro and monocytes withdrawn from animals treated with the same substance showed equally a stimulated activity. This increased phagocytosis was equally inhibited in vitro by the antihistamine, but to a lesser degree than the inhibition of the histamine stimulated phagocytosis. The above observations suggest that the stimulating action of the 1,4-dimethyl-7-isopropyl-bicyclo-decapentane is a direct action on the monocytes rather than an indirect one caused by activation of latent histamine. Experiments also show the possibility of stimulation of the cellular defense mechanism, by appropriate treatment.

STUDIES ON THE EFFECTS OF PHAGOCYTIC STIMULATION ON MICROBIAL DISEASE: III. THE INFLUENCE OF ANTIHISTAMINES AND 1,4-DIMETHYL-7-ISOPROPYLAZULENE ON EXPERIMENTAL TUBERCULOSIS—PRELIMINARY EXPERIMENTS

1955 ◽  
Vol 1 (6) ◽  
pp. 461-469 ◽  
Author(s):  
Béla Gözsy ◽  
Laszló Kátó
Keyword(s):  
Defense Mechanism ◽  
Experimental Tuberculosis ◽  
Toxic Agent ◽  
Histamine Production ◽  
Host Parasite Relationship ◽  
Parasite Relationship ◽  
Antihistamine Drug ◽  
Host Parasite ◽  
The Given ◽  
Reticulo Endothelial System

Albino mice were infected intravenously with Mycobacterium tuberculosis var. bovis (Ravenel strain). The animals treated with the given antihistaminic substance died significantly sooner than the non-treated control animals. In a similar experiment, the deteriorating effect of antihistamine drug on experimental tuberculosis in guinea pigs was demonstrated. On the basis of previous experiments, it is supposed that the physiological stimulation of the defense mechanism by histamine has been hampered in its function. The administration of 1,4-dimethyl-7-isopropylazulene, which is believed to be a non-toxic agent simulating histamine production, prolonged the life of infected animals. When antihistamine was given in addition to 1,4-dimethyl-7-isopropylazulene, the deteriorating effect of the antihistamine was inhibited. Results are discussed in terms of whether the host–parasite relationship can be favorably influenced by means of a stimulant of the reticulo-endothelial system.

STUDIES ON THE EFFECTS OF PHAGOCYTIC STIMULATION ON MICROBIAL DISEASE: V. STIMULATION OF PHAGOCYTIC ACTIVITY OF MONOCYTES AGAINST TUBERCLE BACILLI, STRAIN BCG

1956 ◽  
Vol 34 (3) ◽  
pp. 571-579 ◽  
Author(s):  
Béla Gözsy ◽  
László Kátó
Keyword(s):  
Phagocytic Activity ◽  
Guinea Pigs ◽  
Saline Solution ◽  
Defense Mechanism ◽  
Direct Action ◽  
Intraperitoneal Administration ◽  
Cellular Defense ◽  
Appropriate Treatment ◽  
Stimulation Of

Monocytes were obtained by the washing of the peritoneal cavity of guinea pigs with Hanks' solution six days after intraperitoneal administration of a saline solution containing glycogen. Phagocytosis of tubercle bacilli (BCG strain) was studied after a one hour incubation at 37 °C. under the influence of histamine and 1,4-dimethyl-7-isopropyl-bicyclo-decapentane, which latter substance had shown a beneficial influence on the outcome of experimental tuberculosis. Histamine increased the phagocytic activity of monocytes, within the limits of 1 μgm. to 10 μgm per ml. This stimulation was inhibited in vitro by a synthetic antihistamine substance. Fifty and 100 μgm. per ml. histamine decreased the phagocytosis of tubercle bacilli (BCG) by the monocytes. Monocytes withdrawn from histamine treated guinea pigs showed no stimulated activity. From 0.5 to 100 μgm. per ml. of 1,4-dimethyl-7-isopropylbicyclo-decapentane stimulated the phagocytic activity of monocytes against tubercle bacilli (BCG) in vitro and monocytes withdrawn from animals treated with the same substance showed equally a stimulated activity. This increased phagocytosis was equally inhibited in vitro by the antihistamine, but to a lesser degree than the inhibition of the histamine stimulated phagocytosis. The above observations suggest that the stimulating action of the 1,4-dimethyl-7-isopropyl-bicyclo-decapentane is a direct action on the monocytes rather than an indirect one caused by activation of latent histamine. Experiments also show the possibility of stimulation of the cellular defense mechanism, by appropriate treatment.

Plasmodium falciparumgrowth inhibition by human plateletsin vitro

Parasitology ◽  
1989 ◽  
Vol 99 (3) ◽  
pp. 317-322 ◽  
Author(s):  
F. Peyron ◽  
B. Polack ◽  
D. Lamotte ◽  
L. Kolodie ◽  
P. Ambroise-Thomas
Keyword(s):  
Growth Inhibition ◽  
Human Platelets ◽  
Activated Platelets ◽  
Erythrocyte Lysis ◽  
Host Parasite Relationship ◽  
Parasite Relationship ◽  
Host Parasite ◽  
Oxygen Metabolites

SummaryPlatelets take an active part in immunological processes as well as in haemostasis, especially in the host-parasite relationship. Our aim is to assess the growth ofPlasmodium falciparum, cultured in human erythrocytes in the presence of fresh washed human platelets, since thrombocytopaenia is frequently observed during malarial infections. Our results show that platelets induce a dose-related growth inhibition ofP. falciparum. Both proliferation and maturation of intraerythrocytic stages of the parasite are inhibited. This growth inhibition is triggered by the parasite itself as neither specific antibodies nor any other components are needed to activate platelets. Activated platelets are directly toxic since complement is not involved. Furthermore, inhibition is not mediated by erythrocyte lysis or by toxic oxygen metabolites. Platelets induce an inhibition ofP.falciparumgrowth, at leastin vitro, although the importance of their role playedin vivoin malarial immunity has yet to be evaluated.

Interactions between mosses (Bryophyta) and fungi

2006 ◽  
Vol 84 (10) ◽  
pp. 1509-1519 ◽  
Author(s):  
Marie L. Davey ◽  
Randolph S. Currah
Keyword(s):  
Host Cell ◽  
Mycorrhizal Fungi ◽  
Host Responses ◽  
Fungal Propagules ◽  
Parasite Relationship ◽  
Cellular Specificity ◽  
Host Parasite ◽  
Highly Evolved

A taxonomically diverse suite of fungi interacts with bryophytes as pathogens, parasites, saprobes, and commensals. Necrotrophic pathogens such as Tephrocybe palustris (Peck) Donk and Nectria mnii Döbbeler form patches of moribund gametophytes in otherwise healthy mats of mosses. These pathogens exhibit different methods of host cell disruption; N. mnii appears to displace the host cell protoplast with intracellular hyphae, while T. palustris causes host protoplast degeneration. Host responses to infection by bryopathogens are also variable. Host–pathogen relationships can be highly evolved, as in Bryophytomyces sphagni (Navashin) Cif., in which fungal propagules replace the bryophyte spores, and exploit the explosive dispersal mechanisms of the Sphagnum host. Bryophilous parasites tend to exhibit high tissue or cellular specificity with varying host specificity. For example, Octospora similis (Kirchstein) Benkert infects the rhizoids of species of Bryum, and Discinella schimperi (Navashin) Redhead specifically colonizes the mucilage producing cells of stems of Sphagnum squarrosum Crome. Eocronartium muscicola (Pers.) Fitzp. demonstrates a highly evolved host–parasite relationship in which the basidiocarp displaces the sporophyte and is fed directly by the gametophyte through specialized transfer tissues. Fungi such as Oidiodendron maius Barron are capable of decomposing moss cell walls that are generally resistant to decomposition because of their polyphenolic component. Mycorrhizal fungi, including Glomus, Suillus, and Endogone, have not been observed to form functional, nutrient-exchanging mycorrhizal interfaces with bryophytes, rather, they function as saprobes on moribund and senescent gametophytes. Finally, endophytic fungi may provide bryophyte hosts with greater tolerance to extreme pH or promote vegetative growth. In vivo observation of bryophyte–fungus interactions has provided insight into the types of interactions that occur; however to further understand the physiology, anatomy, and etiology of these interactions, it is necessary to culture bryophilous fungi in vitro and create artificial axenic systems for study.

scholarly journals Host-Parasite Relationship in Cystic Echinococcosis: An Evolving Story

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Alessandra Siracusano ◽  
Federica Delunardo ◽  
Antonella Teggi ◽  
Elena Ortona
Keyword(s):  
Cystic Echinococcosis ◽  
Public Health Problem ◽  
Major Public Health Problem ◽  
Host Parasite Relationship ◽  
Parasite Relationship ◽  
Recent Developments ◽  
Host Parasite ◽  
Human Cystic Echinococcosis

The larval stage ofEchinococcus granulosuscauses cystic echinococcosis, a neglected infectious disease that constitutes a major public health problem in developing countries. Despite being under constant barrage by the immune system,E. granulosusmodulates antiparasite immune responses and persists in the human hosts with detectable humoral and cellular responses against the parasite.In vitroandin vivoimmunological approaches, together with molecular biology and immunoproteomic technologies, provided us exciting insights into the mechanisms involved in the initiation ofE. granulosusinfection and the consequent induction and regulation of the immune response. Although the last decade has clarified many aspects of host-parasite relationship in human cystic echinococcosis, establishing the full mechanisms that cause the disease requires more studies. Here, we review some of the recent developments and discuss new avenues in this evolving story ofE. granulosusinfection in man.

scholarly journals Interactions between Leishmania mexicana mexicana promastigotes and amastigotes and murine peritoneal macrophages in vitro

1983 ◽  
Vol 78 (2) ◽  
pp. 135-146 ◽  
Author(s):  
Gabriel Grimaldi Junior ◽  
Suzana Corte-Real ◽  
Rosa T. de Pinho ◽  
Pamela L. Moriearty
Keyword(s):  
Cell Loss ◽  
Peritoneal Macrophages ◽  
Time Intervals ◽  
Single Strain ◽  
Parasite Survival ◽  
Parasite Relationship ◽  
Infected Cells ◽  
Parasite Multiplication ◽  
Host Parasite

Unstimulated adherent mouse peritoneal cells were cultured in vitro and infected with equal numbers of a single strain of Leishmania m. mexicana amastigotes (AM), virulent promastigotes (VP), avirulent promastigotes (AVP) and fixed promastigotes (FP). Duplicate May-Grünwald-Giemsa stained coverslips were examined at time intervals up to 13 days. By 3 hr post infection, the number of macrophages containing parasites varied between 60.5% (VP) and 84% (AM) for macrophages exposed to living parasites, compared to 6.5% for macrophages exposed for FP. However, variable numbers of parasites showed degenerative changes by 3 hr, and the number of macrophages containing morphologically intact parasites varied significantly between cells infected with AM (84%) and those infected with VP (42%) or AVP(40%). The mean number on intacte parasites/macrophage also differed significantly between AM-infected cells and living or fixed promastigotes-infected cells. Quantitation of intact and degenerated parasites indicated parasite multiplication, as well as destruction, in VP-infected cells and parasite survival and multiplication in AM-infecte monolayers; in contrast no evidence of parasite multiplication was seen in AVP-infected cells. Changes in the mono layer itself (cell loss and macrophage vacuolization) were also evaluated. These results suggest that crucial events determining the outcome of infection occur in the host-parasite relationship during the fist 24 hours of infection. These events are apparently influenced not only by parasite or host strain but by environmentally induced variation within a given strain.

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