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Biomedical subjects

J S Goodwin

Publications and source records attributed to J S Goodwin.

At least 199 records · Page 11Linked to original sources

Immunological responses of healthy elderly population.

We measured in vitro mitogen responses, delayed hypersensitivity skin tests, circulating immune complexes (CIC) and three autoantibodies in 279 healthy and 24 chronically ill individuals over 65, and in young controls. The elderly individuals had previously undergone a complete medical examination and laboratory screening tests, and were on no medications. Compared to the results of 180 young controls tested concurrently, the healthy elderly individuals had significantly depressed PHA responses and skin test responses. In addition, CIC and autoantibodies were increased in the healthy elderly group compared to young controls. There was no difference in PHA or skin test responses between the healthy and chronically ill elderly subjects, suggesting that the major determinant of depressed cellular immunity in the elderly is age per se and not age-associated diseases. Within the elderly population, aged 65-94, there was a significant decrease in PHA response with age. Previously it has been reported that correlations exist between measurements of cellular immune response (mitogen response and skin testing) and manifestations of autoimmunity (CIC or autoantibodies) in elderly subjects. However, in this well characterized healthy elderly population we could not verify an association between the cellular immune response and either autoantibodies or immune complexes. In addition, was no increased prevalence of autoantibodies in subjects with CIC.

Aged↗

Response to pneumococcal vaccine in the elderly: no enhancement by indomethacin.

We investigated whether indomethacin administration would augment the antibody response to pneumococcal vaccine in a group of healthy elderly individuals. There was no significant difference in mean increases in antibody levels to 12 pneumococcal polysaccharide types between the 20 subjects who received indomethacin 25 mg q.i.d. for five days after immunization and the control subjects not receiving indomethacin. In addition, there was no correlation within this group of 40 individuals between three measures of immune function (absolute lymphocyte count, delayed hypersensitivity testing, and response to phytohemagglutinin) and the antibody response to the pneumococcal vaccine.

Adjuvants, Immunologic↗

Effect of physical stress on sensitivity of lymphocytes to inhibition by prostaglandin E2.

Physical stress is associated with depressed cellular immune function. We have found that lymphocytes from subjects undergoing either of 2 stressful events, cardiac surgery or childbirth, are more sensitive to inhibition by PGE2. For example, the concentration of PGE2 required for 50% inhibition of 3H-thymidine incorporation (ID50) into phytohemagglutinin-stimulated lymphocytes from patients undergoing cardiac surgery went from 1.5 X 10(-8) M on the day before surgery to 3 X 10(-9) M on the day after surgery. This increase in sensitivity to PGE2 was accompanied by a significantly decreased lymphocyte proliferative response (27 to 68% of control, depending on mitogen dose) and a 50% increase in the percentage of E rosette-positive cells with receptors for the Fc portion of IgG. The increased sensitivity to PGE and the depressed mitogen responses returned to preoperative values by day 10. The depressed mitogen responses of the postoperative patients were completely restored to normal by removal of glass-adherent cells before culture. In addition, the responses of the postoperative patients and the women in labor were partially restored by the addition of indomethacin, a prostaglandin synthetase inhibitor, to the cultures. Thus it would appear that physical stress causes lymphocytes to become more sensitive to prostaglandin E2, and the increased sensitivity to inhibition by this immunomodulator is responsible in part for the depressed cellular immune function after physical stress.

Cell Adhesion↗

Suppression of lymphocyte proliferation by human tumor cells grown in short term cultures.

We studied the effect of human tumor cells grown in short term cultures on the proliferative response fo normal human peripheral blood mononuclear cells (PBMC) to mitogens and alloantigens. In 6 or 7 short term cancer cell lines studied, the addition of 10(3) cells to mitogen- or alloantigen-stimulated cultures of 10(5) PBMC caused from 20 to 60% suppression of 3H thymidine incorporation. Cells from short term cultures established from biopsies of normal skin did not suppress at these concentrations. The suppression was not due to a change in kinetics, or to a decrease in viability or recovery of either the tumor cells or PBMC in the cultures. Prior treatment of tumor cells with mitomycin C abrogated the suppression, while prior X-irradiation with 1,000, 2,000 or 3,000 rads had no effect. One of the tumor cells caused suppression when separated from the PBMC by a cell-impermeable membrane while another line required cell-to-cell contact for suppression.

Cell Membrane Permeability↗

The nature of the prostaglandin-producing mononuclear cell in human peripheral blood.

The purpose of this investigation was to identify the human peripheral mononuclear cell responsible for PGE production. The prostaglandin-producing cell had the following characteristics: (1) was glass adherent; (2) was removed by techniques that effectively removed phagocytic cells (carbonyl iron); and (3) was not an E-rosette cell. Furthermore, the peripheral mononuclear cells that contain cytoplasmic PGE by indirect immunofluorescence also ingest latex particles. B and T lymphoid cell lines did not produce large quantities of PGE. Mononuclear cells separated on discontinuous BSA gradients varied greatly in their ability to produce prostaglandin (low density > high density). These data constitute strong evidence that the majority of PGE produced in peripheral mononuclear cell suspensions emanates from a population of low-density monocytes.

Cell Adhesion↗

A case of Guillain-Barré syndrome with immunologic abnormalities.

Guillain-Barré syndrome and the nephrotic syndrome developed in a patient simultaneously. Analysis of renal biopsy by light, immunofluorescent, and electron microscopy showed lipoid nephrosis. T-cell lymphocytopenia, lymphocytotoxic antibodies, depressed lymphocyte mitogenesis, and anergy also complicated the illness. The immunologic abnormalities resolved when the polyradiculoneuritis and lipoid nephrosis remitted. This previously undescribed association illustrates the occurrence of two postulated cell-mediated autoimmune disorders despite the presence of depressed cell-mediated immunity.

Adult↗

Suppressor leukocytes in anergic patients with solid tumors.

Anergic patients with solid tumors were studied for the presence of suppressor cells which could be responsible for their significantly impaired phytohemagglutinin induced lymphocyte proliferation. Three types of suppressor cell assays were measured. First, no increased activity of prostaglandin producing suppressor cells was found in 10 cancer patients. Second, 5 cancer patients did not have significantly increased activity of short-lived suppressor cells in comparison with normal subjects. Third, no enhanced activity of concanavalin A induced suppressor cells was seen in 6 patients. This study emphasizes that the in vitro T cell immunodeficiency in this group of cancer patients was not due to suppressor cells as measured by conventional in vitro assays and emphasizes the potential importance of a loss of responder cells or other suppressor mechanisms in immune deficient patients with solid tumors.

Adult↗