Search PubMed⌕ Search

Biomedical subjects

M Joseph

Publications and source records attributed to M Joseph.

At least 181 records · Page 10Linked to original sources
PubMed1983

[Secondarily infected pneumatocele, eosinophilia and excess production of IgE manifesting as Buckley's syndrome in an adult].

The hyper IgE syndrome develops in childhood and leads to repeated infectious episodes, usually of staphylococcus aureus origin and affecting mainly the skin and pulmonary parenchyma. It may be associated with a predominantly facial atypical dermatitis and more rarely with allergic manifestations. Biological tests show mainly an eosinophilia and a hypergammaglobulinemia E alone without modifications in other immunoglobulin types. Disorders of neutrophil and monocyte chemotaxis are inconstant findings. The initial mechanism of the affection appears related to a deficit in suppressive T function selectively acting on the IgE isotype.

Adult↗
PubMed1983

[Local cellular response to stress of the lower lung].

The cell populations in the alveoli are exposed to the environment and react differently to each type of challenge (mineral particles, toxic gases, infections, antigenic substances. . .). Amongst the best studied of these irritant factors is tobacco smoke which in the long term leads to a number of changes both in the distribution of alveolar cells and also their function and morphology. Amongst acute and sub-acute pathogens, bacterial infections produce a rapid poly-morpho-nuclear neutrophilia and then a lymphocytosis; oxygen and oxidising agents in general lead to a neutrophilia which amplifies the pulmonary parenchymal changes related to the release of toxic metabolites of oxygen. The inhalation of antigenic substances also disturbs the behaviour of alveolar cells: activation of macrophages in the presence of allergy in those sensitized to IgE and immediate attraction of neutrophils preceding a T lymphocyte alveolitis in hypersensitivity pneumonia. It is possible to categorise several patterns of reaction in intra-pulmonary cells when challenged by some insult, a direct cytotoxic action, the accumulation of inflammatory cells and immunological competence corresponding to the concept of "a neutrophil alveolitis" or a "T cell alveolitis" with the development of emphysematous lesions. An understanding of the cellular make-up present in the alveoli when reacting to an external pathogen enables a better approach to the pathophysiological mechanisms in question.

Air Pollutants↗
PubMed1983

Immunologic response of athymic rats to Schistosoma mansoni infection. II. Antibody-dependent mechanisms of resistance.

The responses of congenitally athymic rats to Schistosoma mansoni were compared to thymic reconstituted, heterozygous littermate controls, and inbred Fischer rats. The mechanisms of the impaired resistance of athymic rats to initial exposure and re-exposure to S. mansoni were investigated by the study of various parameters of antibody response. The uninfected athymic animals demonstrated normal levels of total IgM but reduced levels of total IgG2a and IgE. After infection with S. mansoni, the immunoglobulin increases in athymic rats were less than those observed in heterozygote control rats. In addition, the level of anti-S. mansoni IgG antibody, utilizing ELISA assay, was reduced. Furthermore, the functional avidity of the IgG2a antibody, which was produced by the athymic animals, was significantly lower than that of control heterozygote and Fischer animals. Similarly, the levels of IgE and IgG2a anaphylactic antibodies were reduced in the congenitally athymic animals. After thymic reconstitution and exposure to S. mansoni of the congenitally athymic animals, all of these parameters became similar to the analogous value obtained from exposed heterozygous and homozygous animals. In vitro studies of antibody-dependent cell-mediated cytotoxicity (ADCC) activity indicated that the antibody response of the congenitally athymic animals was characterized by significant reductions in IgE-macrophage-mediated, IgG-eosinophil-mediated, and IgE-eosinophil-mediated cytotoxicity directed against schistosomula. These results, coupled with previously reported in vivo observations, that athymic animals produced antibody that was less capable of transferring resistance in adoptive-challenge experiments, suggest that the mechanisms of impaired resistance in the congenitally athymic rat may involve the failure to develop adequate, functional ADCC mechanisms. As such, these studies suggest a relationship between in vivo resistance and possible in vitro mechanisms of that resistance.

Animals↗
PubMed1982

A practical approach to the treatment of burn shock in childhood.

A simple method of evaluating and treating burn shock has been used with very good results and low mortality. The amounts of fluids given in a specific time and the type of fluids given are dependent upon the evaluation of a few simple observations. We believe that shock is a treatable condition and that 'shock kidney' is preventable. We stress the difficulty of trying to compare the results of two different burn units.

Blood Transfusion↗
PubMed1982

Foetus in foetu.

Explore the source record for details and available documents.

Child↗
PubMed1981

The effect of 2-amino-4-phosphonobutyrate (APB) on acetylcholine release from the rabbit retina: evidence for on-channel input to cholinergic amacrine cells.

The light-evoked release of acetylcholine (ACh) from the rabbit retina was taken as a measure of cholinergic amacrine cell activity. The glutamate analogue DL-(+/-)-2-amino-4-phosphonobutyric acid (APB) prevented the light-evoked release of ACh and also selectively abolished the ON-responses of ganglion cells and the ERG b-wave. It is concluded that the input to cholinergic amacrine cells involves mainly the depolarizing bipolar cells, which subserve ON-channels. L-(+)-stereoisomer of APB was 15 times more potent than the D-(-)-isomer in suppressing ACh release and the b-wave, suggesting that the mechanism of action of APB does not involve antagonism of excitatory amino acids.

2-Amino-5-phosphonovalerate↗
PubMed1981

The interaction of IgE antibody with human alveolar macrophages and its participation in the inflammatory processes of lung allergy.

After the initial observation that human and animal mononuclear phagocytes can be activated into specific killer cells against larvae of the parasite Schistosoma mansoni by seric IgE antibody from infected patients, a possible interaction of IgE with human alveolar macrophages in asthmatic patients was investigated. In vitro, alveolar macrophages from non-atopic individuals can bind monoclonal IgE molecules, as well as IgE antibody from the serum of patients with respiratory allergy. A subsequent contact with anti-IgE antibody or with the specific allergen induces the extracellular release of a variety of mediators, such as lysosomal enzymes, neutral proteases, or superoxide anion. Due to the presence of allergen-specific IgE antibody on the macrophage surface in situ, the same results were obtained in vitro with freshly purified alveolar macrophages from allergic patients. Disodium cromoglycate, corticosteroids, or beta-adrenergic stimulants are strong inhibitors of this specific exocytosis of physiological mediators. The atopic cells formed rosettes with allergen-coated erythrocytes at 4 degrees C, except after pretreatment with aggregated monoclonal IgE or with the allergen.

Antibodies, Monoclonal↗
PubMed1981

Heat-labile and heat-stable anti-schistosomular antibodies in Kenyan schoolchildren infected with Schistosoma mansoni.

Two in vitro cytotoxicity assays using 51Cr-labelled Schistosoma mansoni schistosomula were performed on serum samples collected from 91 schoolchildren infected with S. mansoni from Machakos District, Kenya. One assay, which is believed to detect IgE/antigen complexes, uses unheated serum and human monocytes; the other, believed to detect IgG antibodies, uses heat-inactivated serum and unpurified peripheral blood leucocytes. Analysis of the data was complicated because the children were drawn from two separate studies and the data was extremely variable, probably because of the manner in which infections are acquired under natural conditions. There was a strong, positive regression of intensity of infection on age of the children, and evidence that IgG, but not IgE, activity was related to intensity of infection. There was no clear-cut relationship of IgE and IgG activities with the age of the children, and little evidence of any correlation between IgE and IgG activities within individual children. The implications of this latter dissociation and the possibility of either mechanism acting as the effector mechanism for concomitant immunity in man are discussed in the light of these results.

Adolescent↗
PubMed1981

Histology of the Fernandez reaction. An appraisal.

The early lepromin reaction was studied clinically and histologically in 38 leprosy patients. There was a quantitative and a qualitative difference in the character of the early inflammatory response to lepromin in the different groups of leprosy patients. In tuberculoid patients, the extent and degree of inflammation and the density of lymphocytic infiltration were maximal. In the polar lepromatous group, the inflammatory reaction was far less intense, and lymphocytes were scarce or absent. An intermediate histology was noted in the borderline and indeterminate groups of patients. In 11 patients with negative clinical reactions, the histology showed moderately dense lymphocytic infiltrations. The paucity of the clinical reaction could be due to the injection and localization of the antigen in the mid- and deep dermis. The correlation between early and late lepromin reactivity, both clinically and histologically, in the polar tuberculoid group and the polar lepromatous group was good. In the borderline and indeterminate groups, only the correlation between the early and late histological reactions to lepromin was good. The relationships between the early and late clinical reactions to lepromin showed marked variation. It is suggested that the early reaction is as good an indicator of lepromin reactivity as the late reaction in all forms of leprosy but only if it is assessed histologically.

Adolescent↗
PubMed1981

Evidence for IgE-dependent cytotoxicity by rat eosinophils.

Human and rodent eosinophils have been shown previously to act as effector cells against Schistosoma mansoni schistosomula by ADCC mechanisms involving IgG antibodies. The present work brings novel evidence for the existence in rat schistosomiasis of an IgE-eosinophil dependent cytotoxicity mechanism. The role of IgE antibodies present in the rat serum after 6 weeks of infection was clearly established by immunoadsorption and inhibition experiments, whereas the participation of IgG and complement in this system could be ruled out. Mast cell products, including ECF-A tetrapeptides, appear to play an essential role in significantly increasing eosinophil cytotoxicity. A kinetic study of the IgG-dependent cytotoxicity mechanism previously described and of this IgE-mediated mechanism according to rat schistosomiasis revealed the preeminent role played by IgG antibodies in early infection, whereas IgE predominated after 6 wk of infection. The possible significance of IgE-eosinophil cooperation in ADCC mechanisms in parasite and nonparasite models is discussed.

Animals↗
PubMed1981

Macrophage triggering by aggregated immunoglobulins. I. Delayed effect of IgG aggregates or immune complexes.

Rat peritoneal macrophages in serum-free cultures were triggered to release lysosomal enzymes or plasminogen activator and to incorporate glucosamine upon exposure to rat IgG that was nonspecifically aggregated after heating or by dimethylsuberimidate cross-linking or was specifically complexed by the corresponding antigen using preformed BSA-anti-BSA immune complexes. A lag period of 6 hr was observed before the increase in enzyme release or in glucosamine uptake. Although chemically prepared dimers of IgG were found sufficient to trigger the macrophages, both enzyme release and glucosamine incorporation increased with the size of the IgG aggregates. Similarly, immune complexes in IgG antibody excess (Ag/Ab ratio 1:32) were more efficient than complexes prepared at equivalence or in antigen excess, which suggests that the size of the aggregates is an important parameter of macrophage triggering. The participation of the macrophage Fc receptor for IgG in IgG-dependent macrophage triggering is suggested by similar findings using a first exposure of the cells to rat IgG then the cross-linking the cell-bound immunoglobulin by purified anti-rat IgG or the F(ab')2 fragment of it. Macrophage function in inflammatory reaction might thus be modulated by the size of IgG immune complexes.

Animals↗
PubMed1981

In vitro killing of S. mansoni schistosomula by lymphokine-activated mouse macrophages.

Inflammatory macrophages from mice i.p. injected with FCS 24-hr before harvesting, activated by partly purified MAF from Con A-stimulated spleen cells, were shown to kill an average of 60.9% (SE +/- 5.3) of the parasites in cultures of Schistosoma mansoni schistosomula. On the contrary, resident macrophages were not cytotoxic under the same conditions. The degree of macrophage activation for the killing was dependent upon both lymphokine concentration and time of incubation in lymphokine. The capacity of macrophages to be activated to kill schistosomula as well as the schistosomulicidal activity of the lymphokine-activated macrophages were short-lived properties. The killing was strongly influenced by the effector-to-target ratio. The results are consistent with other data on the immune response in experimental infection and particularly the development of the delayed hypersensitivity. Therefore, among the immune mechanisms that participate in immunity to reinfection, cell-mediated immunity that involves inflammatory macrophages should no longer be restricted to microorganisms and protozoans and could be extended to multicellular parasites like schistosomes.

Animals↗