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Biomedical subjects

H O Besedovsky

Publications and source records attributed to H O Besedovsky.

At least 55 records · Page 3Linked to original sources
PubMed1985

Lymphoid cells produce an immunoregulatory glucocorticoid increasing factor (GIF) acting through the pituitary gland.

Products are released in vitro by mitogen stimulation of human peripheral blood mononuclear cells or rat spleen cells which increase corticosterone blood levels when injected into normal rats. We report that an almost pure population of human peripheral blood lymphocytes in mixed lymphocyte culture stimulated with phytohaemagglutinin also produces a glucocorticoid increasing factor(s). The product equivalent to the amount released by 5 X 10(5) cells increased corticosterone levels four-fold and also increased ACTH levels. When rats were hypophysectomized or treated with dexamethasone to block ACTH output, no corticosterone increase was noted following administration of glucocorticoid increasing factor(s) (GIF). Similar results were obtained with supernatants of rat spleen cells stimulated with concanavalin A. We conclude that GIF has no direct action on the adrenals in vivo and that a functional pituitary gland is essential for its action. The presented data taken together with those described earlier suggest the existence of a glucocorticoid associated immunoregulatory feedback circuit.

Adrenocorticotropic Hormone↗
PubMed1985

Immune-neuroendocrine interactions.

Concepts and facts concerning immune-neuroendocrine interactions are discussed. The immune response elicits endocrine, autonomic, and brain functional changes. These changes can be mediated by soluble factors released by activated immunologic cells. As a result of these immune-neuroendocrine interactions the content of powerful agents such as hormones, neurotransmitters, and neuropeptides in the microenvironment of immunologic cells is modified. This leads to external immunoregulatory signals imposed upon autoregulatory mechanisms.

Adrenal Cortex↗
PubMed1982

Sympathetic immunoregulation: difference between high- and low-responder animals.

A quantitative relationship is reported between the magnitude of the immune response of rats to sheep red blood cells and diminution of splenic norepinephrine (NE). A decrease in concentration and content of NE in the spleen on day 3 after immunization was evident in both high- and low-responder animals, whereas a diminished concentration of NE persisted only in the high responders. This continuing NE diminution in high-responder animals is associated with increase in spleen weight, probably attributable to blood accumulation. These findings are consonant with the concept that the sympathetic nervous system is involved in immunoregulation.

Animals↗
PubMed1979

Role of prethymic cells in acquisition of self-tolerance.

The sequential character of T-lymphocyte development as it pertains to the stage at which self-tolerance is acquired was investigated. Three phases were studied, defined here as prethymic, intrathymic, and postthymic as determined by the timing of thymus implantation. The model utilized was the temporal pattern of skin graft rejection in thymusless BALB/c nude mice implanted with allogeneic, C57BL/6J, or syngeneic thymuses before or after skin grafting; in some instances, F(1) hybrid spleen cells were also given to newborns or young adults. These experiments in nude mice showed that, (a) self-tolerance could be established despite the absence of the host's own haplotype in the implanted thymus; (b) recently emigrated postthymic cells could already discriminate self from non-self; (c) specific neonatal tolerance could be induced in nudes by inoculation of F(1) hybrid cells; (d) nudes showed a higher capacity for induction of neonatal tolerance than did normal littermates. These findings indicate that the process of self-tolerance in the T cell's lineage begins during the prethymic state early in ontogeny.

Animals↗
PubMed1979

Antigenic competition between horse and sheep red blood cells as a hormone-dependent phenomenon.

Various mechanisms for understanding antigenic competition have been proposed, such as macrophage availability, suppressor cells and their soluble products. In view of the regulatory function of some hormones on the immune system, the role of immunosuppressive adrenal corticosteroids in antigenic competition was investigated. When horse red blood cells (HRBC) were injected into rats a five-fold increase in corticosterone blood levels was measured by day 6 and a strong decrease was noted on day 11. In animals injected with HRBC and on day 6 with a second antigen (sheep red blood cells, SRBC), the corticosteroid level was high on day 11. Such high levels are immunosuppressive. To impede such increases in adrenal hormone levels, rats were adrenalectomized. Adrenalectomized or sham-operated animals receiving SRBC only showed no difference in plaque-forming cell (PFC) numbers. All sham-operated rats injected first with HRBC and 5 days later with SRBC showed the expected antigenic competition. Adrenalectomized rats also injected with both antigens sequentially had a five fold increase in number of PFC when compared with the sham-operated controls which had received both antigens. A detailed analysis of these data revealed that a proportion of adrenalectomized animals had PFC numbers within the normal range. In vitro, hydrocortisone enhances the response of spleen cells when only one antigen (SRBC) is present. Prior addition of the unrelated antigen (HRBC) impedes this enhancement. Thus, in a hydrocortisone-enriched culture medium, the presence of the first antigen can interfere with the immune response to the second unrelated antigen, mimicking in vitro a condition of antigenic competition. These findings indicate that hormones may have a role in antigenic competition.

Adrenal Cortex Hormones↗
PubMed1977

Hormonal control of neutrophil chemotactic activity in the rat vagina.

A sexual-hormone-dependent neutrophil chemotactic factor(s), operative under physiological conditions, is described. Rat vaginal washouts were shown to be both chemotactic and chemokinetic for rat neutrophils in vitro, whereas macrophages were not attracted. Peak activity was observed at the end of estrus and preceded maximal neutrophil infiltration in the vagina. In order to mimic these events, gonadectomized animals were treated with estradiol for a week. They showed a similar peak of chemotactic activity 30-36 h after estradiol withdrawal, accompanied by a massive neutrophil accumulation. These data suggest that a decrease in estradiol level permits the expression of the chemotactic signal. There was no evidence for chemotaxis and/or migration inhibitors before and during estrus or during long-term estradiol treatment of gonadectomized rats. Induced neutrophil accumulation in the peritoneal cavity and chemotactic responsiveness of these cells in vitro were similar in all stages during the estrus cycle. Estradiol, progesterone, testosterone, and hydrocortisone neither promoted nor significantly inhibited the neutrophil migratory behavior over a wide range of concentrations. Our experiments suggest that the periodic neutrophil accumulation in the rat vagina after estrus is triggered by locally expressed chemotactic mechanisms that are controlled by sexual hormones. The data provide the first evidence that hormonal changes can control chemotactic factors and thus indirectly control cell migration.

Animals↗
PubMed1975

Failure of "thymus factor" to restore transplantation immunity in athymic mice.

Implantation of cell impermeable Millipore chambers containing thymuses from normal newborn donors into athymic mice does not confer on them the capability to reject allogeneic skin grafts. The same deficiency is manifested when skin grafted female nude mice are pregnant of foetuses with normal thymuses. These data are thus in sharp contrast to those previously reported for thymic factors reconstituting neonatally thymectomized mice.

Animals↗
PubMed1975

Role of the thymus in programming of neuroendocrine functions.

Specific derangements of thyroid and gonadal functions were observed in athymic nude and neonatally thymectomized mice. Such endocrine alterations are already established during the perinatal period and maintained through adult life. Passive transfer of lymphoid cells from normal donors does not prevent such alterations. In nude mice thymus implantation at birth fully reconstitutes oestrogenic function, but thyroid and progestational functions remain defective. Peripheral endocrine glands (thyroid, adrenals and ovaries) respond normally to ACTH, TSH and LH. Thus the thymus may well have a basic role in the organization of the adult hypothalamus-pituitary axis for thyroid and sexual functions.

Adrenal Glands↗