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Biomedical subjects

H Permin

Publications and source records attributed to H Permin.

At least 19 recordsLinked to original sources
PubMed1992

[Clinical use of intravenous immunoglobulin IgG].

Intravenous human immunoglobulins (IVIG) are valuable in the treatment of several immunodeficiency and autoimmune diseases. The classic, well-known indications are primary hypogammaglobulinaemic conditions, immune thrombocytopenia and Kawasaki's syndrome. IVIG's content of specific antibodies toward a series of known, pathogenic microorganisms has led to the treatment of a number of infectious conditions and IVIG has a documented effect on AIDS in children, prophylactically in cases with potentially life-threatening CMV infections in certain types of transplants and prophylactically in hypogammaglobulinaemic patients with the most common variety of leukaemia, chronic lymphocytic leukaemia. Immunotherapy with IVIG in diseases of autoimmune character such as acute and chronic demyelinating neuropathy has recently shown promising results and encouraging reports have been published in the treatment of severe, steroid-dependent asthma, juvenile chronic arthritis and systemic vasculitis and dermatomyositis where IVIG possibly has a favourable immunomodulating effect on the patient's immune response. Future treatment will probably consist of polyvalent immunoglobulins as well as monoclonal or recombinant monovalent antibodies.

Autoimmune Diseases↗
PubMed1991

Bacteria-induced histamine release from human bronchoalveolar cells and blood leukocytes.

Histamine release induced by Staphylococcus aureus was examined in cells obtained by bronchoalveolar lavage (BAL) in non-atopic individuals. Approximately half of the individuals responded with mediator release to the bacterium, and the release was found to be time- and concentration dependent. No difference was found between the patients who responded and those who did not respond in regard to age, sex, smoker/non-smoker, % recovery of BAL-fluid, total cell count, differential cell counts, histamine content per mast cell, or diagnoses. Also stimulation of the BAL-cells with the calcium-ionophore A23187 resulted in histamine release. S. aureus-induced histamine release from basophils was examined in leukocyte suspensions obtained from the same individuals, and in all experiments release was found. The dose-response curves were similar to those obtained with BAL cells. The bacteria-induced mediator release from superficially lying cells in the airways epithelium might be of importance for the precipitation or exacerbation of bronchial asthma in respiratory tract infections.

Adult↗
PubMed1991

Cytokine-induced histamine release from basophils of AIDS patients. Interaction between cytokines and specific IgE antibodies.

Basophil leukocytes obtained from AIDS patients, allergic patients and healthy controls were stimulated in vitro with interleukin 4, lymphotoxin, tumour necrosis factor alpha and interferon gamma to examine the histamine releasing effect. The cytokines caused histamine release from the basophils of approximately half the AIDS patients and from 8-17% of the allergic patients. No response was obtained in the control group. Removal of cell surface immunoglobulins abolished the response to cytokines, indicating an Ig-dependent mechanism. Passive sensitization with cell-derived Ig, with Ig deprived of IgE, or with IgG, indicated that cell-bound IgE was responsible for the cytokine-induced histamine release in AIDS patients. This response may be mediated by cytokine-selective IgE antibodies.

Acquired Immunodeficiency Syndrome↗
PubMed1991

HIV antigen-induced release of histamine from basophils from HIV infected patients. Mechanism and relation to disease progression and immunodeficiency.

Basophil leukocytes from 39 HIV-infected patients with various degrees of immunodeficiency and disease progression were stimulated with an HIV antigen preparation. Cells from 19 of 22 patients with AIDS and all of six patients with milder degrees of HIV-related disease showed significant histamine release. In contrast, cells from 11 asymptomatic HIV-infected patients and 11 healthy control persons released no histamine. The histamine release induced by HIV antigen was found to be inversely correlated to the number of CD4 positive T lymphocytes. These results indicate that the histamine release was related to both the clinical stage of disease and the degree of immunodeficiency. Passive sensitization experiments showed that IgE, but not IgG, was responsible for the induction of histamine release, indicating the reaction to be type 1 allergic. The histamine release caused by HIV might be involved in the development of disease because of the immunomodulating properties of this mediator.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Virus enhances IgE- and non-IgE-dependent histamine release induced by bacteria and other stimulators.

Histamine release from human basophil leukocytes was triggered by Staph. aureus, Salmonella enteritidis, non-haemolytic streptococci, or E. coli. Influenza A virus was found to enhance the mediator release and the effect was caused by synergism, since the virus did not induce release of histamine per se. This potentiating effect of the virus was seen both when the bacteria-induced histamine release was IgE-dependent (i.e. patient sensitized to the bacterium) and when the bacterium caused mediator release by a non-immunological mechanism independent of IgE (putative sugar-lectin mediated). Histamine release induced by anti-IgE and calcium ionophore or agarose-beads was also enhanced in the presence of the virus. These findings indicate that influenza A virus potentiates both IgE- and non-IgE-mediated histamine release induced by bacteria and other stimulators.

Bacterial Infections↗
PubMed1990

Cytokine-induced release of histamine from basophil leukocytes from AIDS patients.

Cytokine-induced histamine release from basophil leukocytes was examined in cell suspension from AIDS patients and compared with healthy controls. Cells from approximately half of the AIDS patients, in contrast to none from the control group, showed histamine release after stimulation with interleukin-4 (IL-4), tumor necrosis factor alpha (TNF alpha), lymphotoxin (LT) and interferon gamma (IFN gamma). These cytokines seem to induce histamine release from cells from AIDS patients by interaction with the cell surface immunoglobulins, since removal of the immunoglobulins prior to the exposure of the cytokines completely abolished the response to the cytokines. IL-1 alpha, IL-1 beta, IL-3, colony stimulating factor (CSF) and granulocyte-macrophage-CSF (GM-CSF) caused significant histamine release from cells from a similar number of AIDS patients and controls.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Bacteria and endotoxin enhance basophil histamine release and potentiation is abolished by carbohydrates.

Histamine release caused by anti-IgE, specific antigens and calcium ionophore A23187 was examined in leukocyte suspensions from healthy individuals and patients allergic to house dust mite and birch pollen. Staphylococcus aureus and LPS from Salmonella typhimurium were found to cause a synergistic enhancement of the release. The potentiation of mediator release by the bacteria and the endotoxin depends on a binding to the basophilocyte, followed by a non-transient event, since the potentiating effect persists after preincubation of the cells with the LPS followed by washout and leaving the cells for 30 min at 37 degrees C before stimulation with anti-IgE. The potentiation was abolished or reduced by galactose (10(-7) and 10(-6) M) and N-acetylglucosamine (10(-6) and 10(-5) M), acting by a binding to the basophil cell membrane, demonstrated by the persistence of effect after preincubation and washout of unbound sugar.

Adult↗
PubMed1990

Influenza A virus potentiates bacteria-induced histamine release. Examination of normal individuals and patients allergic to bacteria.

Influenza A virus was found to enhance basophil histamine release induced by Escherichia coli, Salmonella enteritidis, Staphylococcus aureus, Streptococcus pneumoniae and Streptococcus sanguis, but did not per se release histamine. This potentiating effect of the virus was seen both when the bacteria-induced mediator release was IgE-dependent (i.e. patient allergic to bacterium) and when the bacterium caused histamine release by a non-immunological mechanism independent of IgE (putative sugar-lectin mediated). Also histamine release induced by other immunological and non-immunological stimuli, such as anti-IgE, calcium ionophore or agarose beads was enhanced in the presence of the virus. The potentiating effect of the virus on bacteria-induced mediator release might be of importance for the conversion from latent to manifest asthma in upper respiratory tract infections.

Adult↗
PubMed1989

HIV antigen stimulates basophil leukocytes from AIDS patients to release histamine due to type I allergy.

HIV antigen-induced histamine release was examined in leukocyte suspensions from 12 patients with AIDS and 10 healthy controls. Nine of the twelve patients released histamine, while no release was obtained in cells from the control group. The mechanism was examined by removal of immunoglobulins (Ig) from the patient cells before stimulation with HIV antigen, which resulted in an abolition of the histamine release. Transfer of the Ig to cells from normal individuals rendered these cells able to respond to HIV. The removal and fixation of Ig were followed by disappearance and reappearance of the response to anti-IgE. These findings indicate that the histamine release by HIV is caused by a type I (IgE-mediated) reaction.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Staphylococcus aureus and influenza A virus stimulate human bronchoalveolar cells to release histamine and leukotrienes.

Mediator release was examined from superficially lying cells in the airway epithelium obtained by bronchoalveolar lavage (BAL) in 13 non-atopic individuals. The BAL-cells were incubated (20 min, 37 degrees C) with Staphylococcus (Staph.) aureus or with human influenza A virus Staph. aureus was found to release histamine from cells from 7 of the 13 individuals and influenza A virus in 3 of 5 persons. Furthermore, Staph, aureus stimulated the BAL-cells to release leukotriene B4 in 7 of 11 subjects, whereas no release was found by influenza A virus in 7 examined persons. When cells from 4 persons were stimulated with Staph. aureus no release of leukotriene C4 was found. The mediator release caused by bacteria and virus might be of importance for the exacerbation of bronchial asthma in upper respiratory tract infections, since histamine is assumed to increase the epithelial permeability with entrance of allergens and other insulting particles, and leukotriene B4 facilitates airway inflammation.

Adult↗
PubMed1989

Determination of immunoglobulins responsible for histamine release induced by microbial antigens in AIDS patients.

AIDS patients in contrast to healthy individuals show basophil histamine release by stimulation in vitro of their blood leukocytes with Candida albicans (CA) and Herpes simplex virus Type I (HSV-I). Passive sensitization of cells from healthy individuals with the patient serum or surface immunoglobulins (Ig) derived from leukocytes of AIDS patients caused histamine release by the following stimulation of the cells with CA or HSV-I. When IgE was removed from the surface Ig no response was obtained, whereas a removal of IgG did not diminish the response. In contrast, no passive sensitization was obtained by serum derived from healthy individuals. The results show that IgE is responsible for the histamine release caused by CA and HSV-I in AIDS patients.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Epidermal tumour necrosis factor alpha and interleukin 6-like activities in AIDS-related Kaposi's sarcoma. An immunohistological study.

Biopsies from 6 patients with AIDS and Kaposi's sarcoma (KS) in the tumour stage, and 6 healthy controls, were immunohistologically examined for the presence of tissue-bound tumour necrosis factor alpha (TNF alpha) and interleukin 6 (IL-6) in the skin. TNF alpha was demonstrated using specific polyclonal antiserum to human recombinant TNF alpha. IL-6 was visualized indirectly using a polyclonal antiserum to partially purified human crude supernatants of activated human blood monocytes, followed by absorption with recombinant human IL-6. The cytokines were found identically located in epidermal cell membranes in stratum granulosum and spinosum of the epidermis from unaffected skin in both AIDS patients and in controls. Biopsies from KS elements showed markedly increased epidermal staining for both TNF delta and IL-6. It was not possible to detect TNF alpha or IL6 in the endothelial cells of the tumour. The observation of increased amounts of epidermal-bound TNF alpha and IL-6 in AIDS-related KS elements supplements previous studies indicating that the skin plays an active immunoinflammatory role in patients with AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Type I reactions directed against Pneumocystis carinii in AIDS patients.

Type I allergy directed against Pneumocystis carinii (PC) has been investigated in 14 patients with AIDS. The Pneumocystis carinii pneumonia often shows a rapid and severe course, and type I allergy against the parasite might be a pathogenic co-factor in the interstitial lung inflammation. In twelve of the AIDS patients the clinical symptoms and course of illness indicated a PC pneumonia. The basophil histamine release test was used as a sensitive test to detect type I allergy against PC. Eight of the patients showed significant histamine release when stimulated with PC. In contrast, only two patients in the group of 12 HIV antibody-positive homosexual men and none in the control group of 13 heterosexual men released histamine. The histamine release was mediated by an immunological reaction, since the release was abolished and regained by removal from and refixation to the cell surface of the cell-bound immunoglobulins before the antigen challenge. The results suggest an involvement of type I allergy as a pathogenic co-factor in Pneumocystis carinii pneumonia.

Acquired Immunodeficiency Syndrome↗