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Biomedical subjects

R G Slavin

Publications and source records attributed to R G Slavin.

At least 109 records · Page 6Linked to original sources
PubMed1978

A primate model of allergic bronchopulmonary aspergillosis.

Allergic bronchopulmonary aspergillosis (ABA) in man is featured by the presence of IgE skin sensitizing and IgG precipitating antibodies against Aspergillus fumigatus (AF). An animal model of this disease was created. 2 monkeys immunized with AF produced IgG-precipitating antibody. Normal human serum was infused into both immunized and unimmunized monkeys and allergic human serum containing a high titer of IgE against AF was infused into another pair of immunized and unimmunized monkeys. All monkeys then received an aerosol of AF. Lung biopsies were obtained and light microscopic, immunofluorescent and electron microscopic studies were performed. Only the monkey with precipitating antibody to AF who received human allergic serum showed changes which included an interstitial cellular infiltrate containing large numbers of eosinophils, edema of the intra-alveolar spaces, thickening of the alveolar septa, intracellular and interstitial deposits of IgG and IgM and proliferation of collagen fibrils. No evidence of vasculitis was observed. This primate model of ABA should enhance our understanding of the inflammatory response and the immunologic processes in this disease.

Animals↗
PubMed1978

Defective chemotaxis in uremia.

Of uremic patients, 37% demonstrated the presence of CFI in their sera. The serum factor acts directly on leukotatic factors, C5f, C3f, and BF to render them irreversibly inactive. Inhibitory activity was found in five of 16 patients: 37% to 61% for C5f, 25% to 36% for C3f, and 28% to 51% for BF. There is no correlation of this inhibitory activity with BUN or creatinine levels. The presence of this chemotactic inhibitor may be responsible for the increased incidence of infection in uremia.

Aminocaproic Acid↗
PubMed1977

Epidemiologic aspects of allergic aspergillosis.

The incidence of allergic bronchopulmonary aspergillosis (ABA) seems much less in the United States than in Great Britain. The suggestion that there are differences in the atmospheric burden of A. fumigatus prompted the authors to evaluate skin reactivity to A. fumigatus in their clinic population. Immediate skin reactivity was found significantly less than to Alternaria, a common Midwest mold. Because of the association of A. fumigatus with decaying vegetation, compost piles in the St. Louis area were cultured. Hot or working piles were extremely rich in A. fumigatus while cold or finished piles were devoid of this organism. A group of nonatopic organic farmers showed no serum precipitating antibody to A. fumigatus. It is suggested that active asthmatics with immediate skin reactivity to A. fumigatus avoid exposure to working compost piles.

Agriculture↗
PubMed1976

The Jewish Hospital of St Louis Therapeutic Grand Rounds No. 14. Hypersensitivity pneumonitis.

Two examples of immunologically mediated diseases of the lung have been discussed. The first, extrinsic allergic alveolitis, is caused by sensitivity to inhalation of an organic dust. It is largely a restrictive type of lung disease and is probably caused by a combination of type 3 and type 4 allergic reactions. The second disease, allergic bronchopulmonary aspergillosis, is caused by a type 1 and type 3 allergic response to Aspergillus antigen in a basically atopic, generally asthmatic individual. It is vital to keep the diagnostic index of suspicion high so as to recognize these diseases early enough to prevent irreparable tissue damage. Extrinsic allergic alveolitis may masquerade as idopathic pulmonary fibrosis or Hamman-Rich syndrome. Allergic aspergillosis may be called Loeffler pneumonia or PIE syndrome (pulmonary infiltrates with eosiniphilia). Failure to diagnose properly may result in extensive pulmonary fibrosis or bronchiectasis and condemn the patient to a lifetime as a pulmonary cripple.

Antigens↗
PubMed1976

Immunologically mediated lung diseases. Extrinsic allergic alveolitis and allergic bronchopulmonary aspergillosis.

Early recognition and treatment of immunologically mediated diseases of the lung are vital to prevent irreparable damage. Extrinsic allergic alveolitis and allergic bronchopulmonary aspergillosis are often confused but should not be difficult to distinguish. The former is nonatopic and is marked by chills, fever, chest pains, cough, dyspnea, and restrictive pulmonary function. The immunologic hallmark is the presence of precipitating antibody to the suspected antigen. Allergic bronchopulmonary aspergillosis is atopic and is marked by low-grade fever, obstructive pulmonary function, markedly elevated serum IgE levels, and positive immediate and late response on skin tests. Both diseases respond well to early corticosteroid therapy. Prophylactic measures are also important in controlling extrinsic allergic alveolitis.

Animals↗
PubMed1976

Mechanism of inhibition of adoptive transfer of tuberculin sensitivity in acute uremia.

Cell-mediated immunity is reduced in uremia, but the mechanism of this inhibition is poorly understood. To determine the site of inhibition a study of adoptive transfer of cell-mediated immunity was undertaken. Strain 13 guinea pigs were made uremic by ureteral ligation. Lymph node cells were isolated and transferred in the following three ways: Group 1: tuberculin sensitive nonuremic donors to nonimmune nonuremic recipients; Group 2: tuberculin sensitive nonuremic donors to nonimmune uremic recipients; Group 3: tuberculin sensitive uremic donors to nonimmune nonuremic recipients. There was no difference in the skin test responses of the transfer recipients in Groups 1 and 3, even though the uremic donors in Group 3 had lost their skin test reactivity. Transfer of tuberculin sensitivity was not successful in Group 2. These results indicate that the uremic state inhibits previously established skin test reactivity but does not prevent sensitized T lymphocytes from transferring cellular immunity.

Acute Disease↗
PubMed1976

Atopic dermatitis.

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Dermatitis, Atopic↗
PubMed1975

The effect of uremic serum on normal human and guinea pig lymphocytes.

Incubation of normal 51-Cr-labeled human and guinea pig lymphocytes with uremic serum or guanidinosuccinic acid did not cause an increase in 51-Cr release. Electron microscopic examination of these lymphocytes revealed no abnormalities. It is suggested that the lymphocytopenia of uremia is not due to increased destruction of cells but may be a result of redistribution to other body compartments.

Animals↗