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Biomedical subjects

R S Panush

Publications and source records attributed to R S Panush.

At least 127 records · Page 7Linked to original sources
PubMed1980

Effects of bovine serum albumin on normal human lymphocytes.

In the course of other experiments we noted increased tritiated thymidine uptake by normal human peripheral blood lymphocytes (PBL) cultured in medium supplemented with bovine serum albumin (BSA) as compared with human plasmas. We confirmed specific stimulatory effects of BSA and sought evidence supporting antigenicity of BSA for human lymphocytes in culture. The PBL cultured in 0.6%-10% BSA incorporated several fold more [3H]thymidine than did cells in medium alone or in human, dog, rat, or guinea pig serum albumins. Responses were maximal for 1% BSA in 7-day cultures. Nonhuman cells (mouse splenocytes) responded comparably in medium and in human, bovine, dog, rat, andf guinea pig albumins. Human lymphocyte donor plasmas contained agglutinators of sheep red blood cells coated with BSA. Agglutination was inhibited by both BSA and antihuman immunoglobulin. These data established specific in vitro stimulatory effects of BSA and suggested that the explanation for this response is that BSA is antigenic to human PBL. Appreciation of such effects is important in conducting and interpreting tissue culture experimentation.

Animals↗
PubMed1979

Effects of acetaminophen on normal human peripheral blood lymphocytes: enhancement of mitogen- and antigen-stimulated incorporation of tritiated thymidine.

This report describes hitherto unrecognized immunoenhancing properties of acetaminophen on cultured human lymphocytes. The addition of acetaminophen (2.5--300 micrograms/ml) significantly enhanced mitogen-induced blastogenesis. The stimulation of cells by Candida albicans, from individuals who were skin-test positive for antigen and two-way responses of mixed lymphocytes, were similarly augmented. Cells stimulated in the presence of acetaminophen were comparably enhanced in cultures lasting for 24--168 hr. Enhancement of stimulated cells was noted only if the drug was added during the first hours of culture. Exposure of cells to acetaminophen before mitogen stimulation did not enhance responses unless tha cells were simultaneously cultured with mitogen and the drug. Cells obtained from normal subjects before, during and after ingestion of therapeutic amounts of acetaminophen for 3 days, were cultured in a medium without acetaminophen, and did not display increased in vitro responses during or after drug consumption. These data indicated: (1) pharmacological concentrations of acetaminophen significantly enhanced lymphocyte responses to specific, non-specific, soluble and insoluble stimulation in vitro; and (2) enhancement by acetaminophen occurred only when the drug was in contact with cells during the early period of cell activation.

Acetaminophen↗
PubMed1979

Penicillin and cephalosporin immunogenicity in man.

Whether cross-allergenicity exists between the penicillin and cephalosporin antibiotics is controversial. A solid-phase radioimmunoassay was adapted to detect drug-specific IgG, IgM and IgE antibodies. Penicillin and cephalothin-specific serum immunoglobulins were determined in patients' serum before and after a therapeutic course of sodium cephalothin. Changes in IgG, IgM and IgE antipenicillin and anticephalothin antibodies, respectively, occurred and were closely correlated to one another (r = 0.80--0.99, p less than 0.0005), indicating that antibody responses to penicillin and cephalothin were linked. This in vitro assay system should prove useful for further study of clinical drug allergies.

Animals↗
PubMed1978

Effects of fenoprofen and benoxaprofen on human lymphocytes: inhibition of tritiated thymidine uptake.

The effects of the related nonsteroidal anti-inflammatory agents, fenoprofen and benoxaprofen, on in vitro responses of normal human peripheral blood lymphocytes were examined. Drugs caused dose-related inhibition of stimulated cell responses. Fifty percent inhibition occurred at 400 microgram/ml calcium fenoprofen and 250 microgram/ml sodium benoxaprofen. Drugs affected not only responses to soluble phytomitogens but also responses to specific antigens and allogeneic lymphocytes. Numbers of viable cells in cultures with and without mitogens and drugs were similar at beginnings and ends of experiments, excluding drug-related cytotoxicity. Inhibition by drugs was greater when cells were cultured in medium alone than in medium with plasma. Cells that were exposed overnight to drugs and then washed and stimulated did not respond as well as did cells not exposed to drugs. These data indicated that fenoprofen and benoxaprofen exhibited noncytotoxic, incompletely reversible inhibition of nonspecific, specific, soluble and insoluble, mitogen-stimulated lymphocyte responses. These findings may pertain to the anti-inflammatory efficacy of these drugs.

Anti-Inflammatory Agents↗
PubMed1978

Interaction of [14C]acetylsalicylic acid with normal human peripheral blood lymphocytes.

Therapeutic concentrations of acetylsalicylic acid (ASA) have strikingly inhibited in vitro and in vivo mitogen- and antigen-induced blastogenesis by human lymphocytes. These observations may be pertinent to the anti-inflammatory actions of ASA. To investigate further the possible effects of ASA on cellular responses, we studied the in vitro interaction of [14C]ASA with lymphocytes. Results indicated that the [14C]ASA association with cells was (a) proportional to ASA concentrations, (b) non-saturable at high concentrations of ASA, (c) dependent on pH, (d) independent of temperature, (e) dependent on cell concentration, (f) not consistently displaced by unlabelled ASA or other drugs, (g) rapid and unchanged over 1 min to 72 hr incubations and (h) reversed by repeated cell washing. These data confirmed that ASA indeed interacted with lymphocytes. The association was rapid, reversible, pH-dependent and not demonstrably specific under these experimental conditions.

Aspirin↗
PubMed1977

Cell mediated immunity in rheumatoid arthritis: Imparied lymphocyte responsiveness, humoral immunosuppressants, and correlations with clinical status in patients off drug therapy.

Cell mediated immune functions were studied in 17 patients with rheumatoid arthritis (RA) at times off all drug therapy, and were correlated with clinical findings. Cellular immunity was evaluated by (1) skin testing to antigens and (2) measuring peripheral blood lymphocyte (PBL) and effusion lymphocyte tritiated thymidine (3H-TdR) uptake in in vitro cultures containing 20 percent autologous or 20 percent AB plasma and various concentrations of mitogens or antigens. Cutaneous and in vitro reactivity were decreased in RA patients: (1) RA PBL spontaneously incorporated more 3H-TdR than normals; (2) 3H-TdR uptake by RA PBL, cultured in AB plasma, in response to mitogens and antigens was markedly reduced when compared with normals; (3) RA PBL responses were further diminished when cells were cultured in autologous plasmas; (4) effusion lymphocytes similarly often had high unstimulated 3H-TdR uptakes and poor responses to stimulation; and (5) decreased proliferative responses of RA PBL (in AB plasma) correlated with class and stage III-IV, increasing age, number of tender or swollen joints, rheumatoid factor titer, total protein, decreased grip strength, and poor skin test reactivity.

Adult↗
PubMed1976

Effects of acetylsalicylic acid on normal human peripheral blood lymphocytes. Inhibition of mitogen- and antigen-stimulated incorporation of tritiated thymidine.

Since mechanisms for known anti-inflammatory effects of acetylsalicylic acid (ASA) in rheumatic or immunological diseases are poorly understood, we have studied effects of ASA on in vitro responses of human lymphocytes. Viable lymphocytes from normal individuals were cultured sterilely at 10(6) cells/ml in RPMI 1640 supplemented with 20% pooled AB plasma, at 37degreesC, 5% CO2. Replicate cultures were incubated with or without adding ASA and unstimulated or stimulated by PHA, Con-A, PWN, Candida, or SK-SD. Cultures contained greater than 95% mononuclear and greater 80% viable cells before pulsing with [3H]TdR, harvesting, and counting. Results indicated that adding 3-40 mg/100 ml ASA to culture resulted in significant inhibition of mitogen-induced blastogenesis. As little as 5-10 mg/100 ml ASA caused approximately 30% inhibition of [3H]TdR uptake, and virtually complete inhibition occurred with 20 mg/100 ml of ASA. Stimulation of cells from persons who were skin-test positive for Candida and SK-SD by these antigens in vitro was similarly suppressed by ASA. Exposure of cells to ASA before stimulation in medium without ASA still demonstrated time- and concentration-dependent inhibition of blastogenesis. Cells from normal individuals, obtained immediately and several days after orally ingesting therapeutic amounts of ASA (plasma level 23 mg/100 ml), cultured in medium without ASA, stimulated less well to mitogens that did cells obtained from these persons before ASA ingestion. These data show that: (i) therapeutic concentrations of ASA inhibit lymphocyte blastogenesis to both mitogens and antigens; (ii) inhibition was non-cytotoxic and partially reversible; and (iii) cells from normal subjects who had ingested therapeutic amounts of ASA responded less well to mitogens in vitro than before ASA ingestion. These observations are pertinent to clinical investigations of cellular immune response of individuals on drug therapy and to the possible mechanism(s) of anti-inflammatory action of ASA in immunologically mediated diseases.

Antigens, Fungal↗
PubMed1974

Rheumatoid factors.

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Arthritis, Rheumatoid↗