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G Filipp

Publications and source records attributed to G Filipp.

27 records · Page 2Linked to original sources
PubMedDate not supplied

Prevention of experimental immune complex glomerulonephritis by specific inactivation of immunoreactive cells.

In a previous experiment we were able to induce in rabbits a state of specific tolerance against bovine serum albumin (BSA) by pretreatment with highly hot labelled BSA-125 I thus preventing immune complex glomerulonephritis. Despite successful suppression of antibody production, the question remained to be answered if this was due to an nonspecific effect of immunosuppression by radio-iodinated BSA or caused by the elimination of the corresponding lymphocyte clone according to the clonal deletion theory. Therefore, rabbits, rendered tolerant BSA antigen were treated with another antigen, bovine gamma globulin (BCG) and developed classical immune complex glomerulonephritis and vice versa. These results strongly suggest a specific elimination of the effector cell clones only, the exact mechanism of which still remains to be elucidated.

Animals↗
PubMedDate not supplied

Experiments on the role of virus infections in the pathogenesis of bronchial asthma. The role of innate or acquired insufficiency or ergotropic adaptation in the mechanism of genesis of bronchial asthma.

UNLABELLED: The wide mosaic of congruent clinical and experimental observations led to the postulation that the cause of the pharmacological abnormality of the asthmatic patient, i.e. the immensely increased reactivity of the bronchial smooth muscles, is to be sought in an insufficiency of the beta-adrenergic receptor system. It is to be assumed that the so-called asthma diatheses is based inter alia on a genetically determined defect of the adenyl cyclase system. The role of previous infections of the respiratory tract in asthmagenesis should lie--following this working theory--not in a sensitization in the sense of an allergic reaction of the immediate type, but in the formation of a defective beta-adrenergic substance or in a blockade of the beta-receptor. A genetically determined innate defect of the beta-adrenergic receptors, or a defect acquired through infections of the respiratory tract, is hence likely to be the cause of the pathologically potentiated reactivity of the bronchia. It is likely that the infective stimuli--quite apart from this preparatory role--are later capable of triggering asthmatic paroxysms when the vegetative homeostasis is impaired. We know from the experiments of many authors that a blockade of the beta-receptors produced by chemical blocker substances, or by pertussis vaccine or various bacterial substances, results in a significant increase in bronchial reactivity towards histamine, serotonin, acetylcholine and other stimuli. We have shown in our experiments that heat-inactivated adeno viruses and influenza viruses also increase the anaphylactic shock reactivity and the histamine reactivity of the organism. On the basis of this working hypothesis, the pathomechanism of the asthmatic process is as follows in individual asthma forms: 1) In the 'purely" allergic asthma form, the antigen-antibody reaction that occurs after sensitization (i.e. formation of skin-sensitizing allergic antibodies of the class IgE) results in re-formation and release of slow-reacting-substances. RESULT: spasm of the bronchial muscles, asthmatic paroxysm. The expulsion of catecholamines that follows the release of slow-reacting-substances makes a decisive contribution to the reestablishment of the impaired homeostatic balance. It is to be assumed that this form of asthma both symptomatically and causally--using specific desensitization--can be influenced more easily than other forms of asthma with a more complicated pathogenic background. 2) In the second allergically determined form of asthma, we are confronted by the genetically fixed or acquired insufficiency of the beta-receptors in addition to the immunological mechanism. As a result of the innate or acquired blockade of the beta-receptive substance, or the relative dominance of the alpha-receptors, the catecholamines (that physiologically serve to maintain homeostasis) contribute to a protraction, intensification and perpetuation of the bronchial obstruction. In this way the asthmatic circulus vitiosus is complete...

Adenoviridae↗
PubMedDate not supplied

Specific desensitization and its mechanisms.

The following discussion concerns the background of the efficiency of classical desensitization. On the basis of clinical studies and reflections the author strives to bolster his own theory on the induction of immunological tolerance on a consequence of the immunotherapy. He presents other different hypotheses of the classical desensitization therapy. In the second part of the review, the author discusses other methods of the immunotherapy with the aid of manipulated and conjugated allergens, the application of allergen-muramylpeptides of allergen mycoloilmuramylpeptides conjugates, of allergen-pullulan compounds, of conjugates of hapten and hydrophylic polymers. The urea denaturod antigens, the allergoids, etc. etc., also belong to this group. These compounds respectively, conjugates to either suppress the T-helper lymphocytes and/or stimulate the T-suppressor cells. At the end of this review, the author reports on his own experiment on specific immunosuppression with the aid of high hot labelled allergens. He and his group have indeed, in this way, suppressed specifically the synthesis of antibodies as well as the clonal expansion of T-lymphocytes.

Allergens↗
PubMedDate not supplied

Antigen-specific suppression of the experimental immune complex glomerulonephritis in rabbits by means of highly hot labelled antigen.

We succeeded in suppressing almost completely the development of glomerular immune disease in a new experimental model, i.e. in the model of immune complex glomerulonephritis. Previous injection of highly hot labelled BSA was able to prevent very significantly the appearance of kidney injury. This result must be interpreted as the consequence of suppression of the synthesis of anti-BSA-antibody by means of previously applied highly hot labelled BSA. As a consequence of the lack of anti-BSA-antibodies there is no formation of antigen-antibody complexes, no deposition of these complexes in the glomerulus basement membrane, and no development of glomerular immune complex disease. Radioactivity alone (125I coupled to HGH) was not capable of modifying or suppressing the synthesis of antibody and consequently, the formation of antigen-antibody complexes.

Animals↗
PubMedDate not supplied

The synthesis of bradykinin-azoprotein and its effectivity.

Some authors succeded in binding the bradykinin in form of a haptene by an azo-bridge to the human gammaglobulin as a vehicle. In this way, the bradykinin has been supplemented to a complete antigen. The bradykinin as a strongly vasoactive substance causes--after a local intradermal injection--an intensive circumscribed increase of the permeability of the capillaries. If such animals receive an intravenous or intracardiac injection of a 1% Evans blue solution, there is a strong blue colouring in the place where the bradykinin has been applied. The guinea pigs and the rabbits which had been immunized by bradykinin-azo-protein showed a significant decrease in the local accumulation of the Evans blue-solution,, which must be attributed to the immunologic neutralization of the intradermally injected bradykinin by an anti-bradykinin-antibody. The intradermally injected bradykinin is neutralized by the bradykinin-antibody. The intravenous or intracardiac injection of bradykinin causes a strong bronchoconstriction in the guinea pig. In those animals which have been pretreated with bradykinin-azo-protein, either there was no asthmatic dyspnoea at all or a decrease of the bronchial reaction would be found. This result very probably is also caused by the production and the activity of anti-bradykinin antibodies.

Alpha-Globulins↗