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Biomedical subjects

W K Podleski

Publications and source records attributed to W K Podleski.

8 recordsLinked to original sources
PubMed1991

Inhibition of antibody-dependent allergic autocytotoxicity in rheumatoid arthritis by OM-89.

Rheumatoid arthritis (RA) is a disease of multiple etiologies and clinical evidence suggests that a separate variant called "allergic arthritis" induced by food antigens could exist. A missing link in the confirmation of such an observation is a relative lack of a reliable in vitro assay which can confirm the in vivo oral ingestion challenge. Therefore, white blood cells (WBC) from 33 rheumatoid arthritis patients were separated and their disintegration was measured in the presence of specific IgE RAST positive sera and gluten-gliadin antigens. This assay was called the antibody-dependent allergic autocytotoxicity (ACT) test which represents an equivalent of an oral ingestion challenge with food antigens. Control WBC expressed 10-45% disintegration as compared to 75-95% in RA. Preincubation of WBC with OM-89 (immunomodulating fractions of Escherichia coli, OM Laboratories Ltd, Geneva, Switzerland) inhibited significantly antibody-dependent ACT in a dose-related manner (P less than 0.001) in our patients.

Adjuvants, Immunologic↗
PubMed1979

Suppression of mitogen-induced, cell-mediated cytotoxicity by prostaglandin F2 alpha in bronchial asthma.

Prostaglandin F2 alpha (PGF 2 alpha) has a bronchoconstrictive effect on the smooth muscles of the bronchial tree, while a prostaglandin of the E series (PGE) provokes bronchodilatation in bronchial asthma (BA). The PGE series can suppress cytotoxic T lymphocytes and it was expected that PGF2 alpha would have the opposite effect, since similarities exist between microvilli of circulating blood lymphocytes and bronchial smooth muscles. Pharmacological modulation of lymphocytes, using a mitogen-induced, cell-mediated cytotoxicity assay (MICC), showed that PGF2 alpha suppresses cytotoxic activity of lymphocytes in BA patients and normal controls. This observation provides evidence that the spasmogenic effect of inhaled PGF2 alpha on the smooth muscles of the airways does not correspond to expected increased cytotoxicity of the circulating blood lymphocytes in vitro.

Adult↗
PubMed1978

The influence of corticotherapy on mitogen induced lymphocytotoxicity in bronchial asthma.

In a previous study the hyperreactive lymphocytes in bronchial asthma (BA) have been documented by mitogen induced cell-mediated cytotoxicity (MICC). Since MICC was considerably low in patients receiving substantial doses of steroids, further investigation was conducted. BA patients were divided into three groups: the first was given daily steroids, the second was given steroids on alternate days and the third consisted of a longitudinal follow-up study on the same individual being on different doses of steroids. Mixture of blood lymphocytes, phytohemagglutinin and Cr51 labeled target cells (P815/DBA2) were incubated in ratio 10:1 for 12 hours. Subsequently the cytotoxic potential of effector lymphocytes was detected by measuring the Cr51 in the supernatant of reacting cells. It was observed that cytotoxic correction index (CCI = Patient/Control Cytotoxic Index) was significantly lower among those in the first group and when the dose of Prednisone or its equivalent exceeded 40 mg/day. Comparison of the CCI between patients from the first and second groups supports alternate day corticotherapy in BA. Considerable fluctuation of CCI was apparent in the third group. Selected high doses of steroids suppressed MICC. This effect is reversible and offers a new practical in vitro guidance for monitoring an adequate dose of steroids in vivo.

Adrenal Cortex Hormones↗
PubMed1977

Anaphylactic injury--a process of programmed regulation.

Anaphylactic injury is a process of tissue destruction mediated by vasoactive amines secreted by basophils and/or mast cells. A cellular model is proposed involving the immunoregulatory properties of basophils, eosinophils and lymphocytes. The interaction of these cells speaks for programmed control mechanisms, the impairment of which leads to expression of anaphylaxis.

Anaphylaxis↗