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PubMed1994

Mast cells in experimental allergic encephalomyelitis: characterization, distribution in the CNS and in vitro activation by myelin basic protein and neuropeptides.

Mast cells (MC) have been implicated in the pathogenesis of experimental allergic encephalomyelitis (EAE). In order to further evaluate their role, several morphological and functional studies were performed. Semiquantitative counts of histological sections showed a significant reduction in MC numbers in EAE brains. In addition, a higher proportion of EAE MC (about 50-70%) appeared degranulated compared with about 20% degranulation in controls. Central nervous system (CNS) MC exhibited staining properties of connective tissue MC and about 98% of them, both in diseased and control rats, were located in the thalamus. They were not present in the spinal cord and did not relate to EAE lesions. In vitro incubation of peritoneal MC (of connective tissue phenotype) with either MBP, or with neuropeptides such as substance P or bradykinin resulted in release of beta-hexosaminidase and histamine. The latter responses were similar in both EAE and control rats. It is suggested that the decrease in number and in granular content of CNS MC in EAE may reflect prior in vivo activation. The fact that MC were activated by MBP and by neuropeptides in vitro suggests a possible mechanism of MC activation in EAE.

Animals↗
PubMed1990

Modulation of pulmonary bombesin by nicotine and vagotomy.

In pregnant hamsters, three transplacental injections of the ganglionic agonist nicotine resulted in a dose-dependent decrease in the concentration of mammalian bombesin (MB) in the lungs of neonatal (1 day old) animals. This decrease in neonatal MB did not occur if nicotine was given only once during gestation, or when it was given three times in conjunction with the ganglionic antagonist mecamylamine. In one week old animals born of mothers who had been exposed to three doses of nicotine during gestation, lung MB had returned to control levels. When nicotine was injected into neonatal animals, lung MB acutely increased. Right sided vagotomy to young hamsters resulted in an increase in the ratio of lung MB (right vs. left lobe) 1 week after surgery. Administration of nicotine to vagotomized animals resulted in decreased total lung MB and normalization of the MB ratio. Thus, nicotine has a potent modulatory influence on lung MB during fetal and neonatal development and maturation. This influence is also present in young animals that are subjected to partial denervation. Our hypothesis is that the innervation of pulmonary neuroendocrine (PNE) cells influences both PNE cell growth and its synthetic function. PNE MB, which is an epithelial and neoplastic growth factor, may play a role in this response.

Animals↗
PubMed1992

Asymmetrical brain modulation of immune reactivity in mice: a model for studying interindividual differences and physiological population heterogeneity?

Functional brain asymmetry is associated with immune reactivity in mice. This association depends on the immunological parameters tested and on the sex and genetic background of animals. Each individual may be characterized by a paw preference score in relation with a particular immune pattern. The interindividual differences in immune reactivity connected with brain asymmetry give a new insight in the relation brain immunity and may represent a new aspect of population polymorphism.

Animals↗
PubMed1990

Transplantation of pituitary grafts fail to restore immune function and to reconstitute the thymus glands of aged mice.

There is evidence to indicate that the neuroendocrine and immune systems can interact. Thus, neuroendocrine hormones can modulate a variety of immune functions and there have been attempts to manipulate the neuroendocrine system of aged animals to enhance immune function. We have previously shown that the transplantation of a syngeneic pituitary gland under the kidney capsule of young adult mice elevates serum prolactin and enhances immune responsiveness. In the present study pituitary glands were transplanted under the kidney capsule of 22-month-old mice to determine if this maneuver can enhance a number of immunologic parameters. The results demonstrate that aged animals bearing transplanted pituitary grafts for 10 days did not exhibit any enhancement in their primary antibody response to sheep red blood cells, splenic T or B-cell mitogen responsiveness or restoration of thymic architecture. When these immunologic assessments are performed on animals bearing pituitary grafts for 28 days, the IgM and IgG primary antibody responses and splenic T-cell responsiveness are enhanced but repopulation of the thymus still does not occur. Importantly, this enhancement does not restore immunocompetence to levels observed in young mice.

Aging↗
PubMed1993

Acute and chronic stressor effects on the antibody response to sheep red blood cells.

Exposure to inescapable foot-shock 72 h following immunization with sheep red blood cells resulted in a marked suppression of the peak splenic immunoglobulin (Ig)M plaque-forming cell response and plasma antibody titers in CD-1 mice. However, the nature of this effect was influenced by the animal's stressor history. In particular, if mice were initially exposed to a single stressor session immediately or 24 h following antigen treatment subsequent reexposure to the stressor (72 h following inoculation) did not provoke the immunosuppression. Moreover, reexposure to the stressor-related cues elicited a marked immunoenhancement. In contrast, if animals were exposed to a single stressor session 48 h prior to inoculation then later reexposure to the stressor-related cues provoked an immunosuppression. Among mice that had been exposed to a repeated stressor regimen on successive days prior to inoculation, the immunosuppression ordinarily elicited by an acute stressor was absent. Indeed, chronic stressor exposure typically favored potentiation of the immune response. However, the immunofacilitation elicited by the chronic stressor treatment likely was unrelated to the immunoenhancing effects of pairing a stressor with antigenic challenge.

Acute Disease↗
PubMed1989

Immunoregulation by neuroendocrine factors.

The influence of the pituitary gland and of steroid hormones on the lymphoid system was demonstrated experimentally over half a century ago. Observations indicating the possibility of behavioural modification of immunity were also made at about the same time. Although these initial observations were followed by numerous investigations, the lack of sufficient basic knowledge of the endocrine and immune systems and serious methodological difficulties led to contradictions from which no definite conclusions could be drawn. Thus, the idea of neurohormonal-immune interaction fell gradually into disrepute. The remarkable effect of corticosteroids and their analogues on the immune system was regarded as a pharmacological phenomenon, rather than a physiological mechanism. During the past decade, this area gradually again became one of the forefronts of biomedical investigation and recently a number of volumes have been published on the subject of neurohormonal-immune interactions. Because of space limitations, only a brief overview of the subject can be given below and the reader is referred to the cited literature for detailed information.

Animals↗
PubMedDate not supplied

The opioid specificity of beta-endorphin enhancement of murine lymphocyte proliferation.

Beta-endorphin (beta-end) is a potent analgesic peptide which exhibits a variety of pharmacological activities in the central nervous system (CNS) following binding of its N-terminus to specific opioid receptors. Although C-terminal binding sites for this 31-amino-acid peptide have been characterized in CNS tissue, identification of their possible function has been facilitated by studies of beta-end effects on lymphocyte activities. In this communication, we report a detailed analysis of the opioid specificity of the ability of beta-end to enhance T cell mitogen-induced proliferation in unfractionated murine splenocytes. Intact 31-amino-acid beta-end peptides from several species, including human, camel and rat, enhanced concanavalin A-stimulated [3H]thymidine uptake 50-640% in a dose-dependent, naloxone-irreversible fashion. The presence of the C-terminal amino acids was required for the enhancement activity, since met-enkephalin, alpha- and gamma-endorphin, and human beta-end 1-27 were ineffective. Accordingly, the truncated peptides, human beta-end 6-31 and 18-31, were also able to enhance the Con A response. However, human beta-end 18-31 was consistently not as effective as beta-end 6-31 or the intact 31-residue peptide. These data suggest that although the C-terminus contains the primary active sequence, the N-terminus contributes to the overall potency of the effect. In support of this assertion, N-acetylation, which abolishes opioid binding activity, resulted in a reduced magnitude of enhancement. The data suggest that beta-end interacts with a non-opioid receptor which has specificity characteristics strikingly similar to non-opioid receptors characterized in CNS tissue.

Amino Acid Sequence↗
PubMedDate not supplied

In vitro effect of methionine-enkephalin and thymosin on murine expression of Thy1-2 antigen.

The present study investigates the in vitro effect of methionine-enkephalin (Met-Enk) on Thy1-2 antigen density and the interaction between this opioid peptide and a thymic hormone (thymosin fraction V (TFV]. In vitro, it was found that Met-Enk at various concentrations (28.10(-11), 28.10(-10), 28.10(-9) and 28.10(-8) M) had an increased positive effect on the Thy1-2 antigen density of Balb/C mouse thymocytes. This action was observed at all concentrations of Met-Enk. The addition of TFV to Met-Enk thymocyte cultures showed an additive effect of these two hormones. The physiological significance of these observations is that they indicate an interaction between immune and endocrine system functions.

Animals↗
PubMedDate not supplied

Short-term somatostatin infusion affects T lymphocyte responsiveness in humans.

Peripheral blood lymphocytes (PBL) function was analysed in 16 young men with duodenal ulcers after one-hour intravenous infusion of somatostatin (SMS) at a dose of 250 micrograms/h. Proliferative responses of PBL from SMS-treated patients were significantly diminished compared with pre-treatment values, after stimulation with PHA, PWM or Con A. Spontaneous IL-2R expression was moderately increased after SMS infusion but PHA-induced IL-2R expression was not affected by this drug. Alloantigen and autoantigen stimulation of PBL showed no significant changes in the proliferative response after SMS infusion. NK cell activity was similarly unaffected. These observations establish a link between SMS exposure and possible development of immune dysfunction.

Adult↗
PubMedDate not supplied

Natural killer activity in hyperprolactinemic patients.

Several pieces of evidence suggest the existence of a relationship between neuroendocrine and immune systems. Prolactin (PRL) has been demonstrated to modulate some immune responses and its influence seems to be permissive or inhibitory depending on its concentration. Previous studies have reported a reduced natural killer (NK) cell function in patients with hyperprolactinemia. In 36 patients (34 females and 2 males, aged 14-46 years) with hyperprolactinemia (mean +/- SEM PRL 142.2 +/- 42.1 micrograms/l) of tumorous (19 patients) and functional (17 patients) origins, NK activity of peripheral blood lymphocytes (PBL) was studied. Patients had NK cell activity against the K562 cell line which did not differ from that of lymphocytes from 36 age- and sex-matched healthy donors (mean +/- SEM lytic units (LU) 619.0 +/- 103.0 and 531.9 +/- 52.6 respectively). No correlation between PRL levels and LU values was found (r = 0.28). When patients with tumors or functional hyperprolactinemia were separately analysed no difference was found between these two groups (mean +/- SEM LU 690.0 +/- 117.7 vs. 606.0 +/- 148.8). In conclusion, our data demonstrate that neither the elevated PRL levels nor the PRL-secreting tumor per se interfere with the NK system of hyperprolactinemic patients.

Adolescent↗
PubMedDate not supplied

Substance P increases and prolongs increased output of T4 (CD4) lymphocytes from lymph nodes of sheep in vivo: is it a mediator of immunological memory?

There are receptors on lymphocytes for substance P which are found both on small recirculating and on blast lymphocytes. The principal effect of substance P on lymphocytes appears to be a stimulating one, both in vitro and in vivo. The in vivo administration of substance P to sheep by acute infusion into cannulated afferent lymphatics of peripheral lymph nodes has been found to stimulate efferent lymph flow and the output into efferent lymph of both small recirculating and blast lymphocytes. We here report that substance P both enhances and prolongs the enhancement of the output of T4 (CD4) lymphocytes from lymph nodes of sheep in vivo. This output-stimulating effect appears to be specific to T4 (CD4) lymphocytes and is associated with a depressant effect on the output of T8 (CD8) and B lymphocytes. The output-stimulating effect on small T4 (CD4) lymphocytes is quite prolonged, lasting in excess of 96 h after a single 50 micrograms acute infusion. A brief post-infusion depression in T4 (CD4) lymphocyte output is associated with an equally brief, but marked, elevation in the output into efferent lymph of the arachidonic acid metabolite, thromboxane B2. The output-stimulating effect of substance P on blast T lymphocytes is confined to the T4 (CD4) blast lymphocytes. Substance P or a similar molecule may be of value when a specific T4 (CD4) lymphocyte output stimulant effect is desired. A single prior (6 days) acute infusion of substance P into a popliteal lymph node via its cannulated afferent lymphatic produced profound changes in the response to nodal drainage area immunization with killed S. muenchen bacteria. The latent period prior to increased antibody production was abolished, as was the standard post-immunization 'shutdown' period of decreased output of lymphocytes into efferent lymph. These changes were accompanied by a marked and progressive increase in antibody production. The findings reported here suggest substance P-induced long-term potentiation (LTP) of the immune response and raise the question of an involvement of substance P as a major mediator of immunological memory.

Animals↗
PubMedDate not supplied

Resistance of C57Bl/6 mice to immunosuppressive effects of aflatoxin B1 and relationship with neuroendocrine mechanisms.

Aflatoxin B1 (AFB1) a secondary metabolite of Aspergillus flavus and A. parasiticus, is known for its carcinogenicity and immunosuppressive effects. We previously reported on the immunosuppressive effects of AFB1 in Swiss and CD-1 mice. This study concerned the involvement of the hypothalamus-pituitary-adrenal gland axis in the immunosuppressive effects of AFB1 in C57Bl/6 mice. Animals were treated orally with 30, 150 or 750 micrograms/kg AFB1 daily for four weeks. Splenic lymphocytes were assayed to investigate their phenotyping using flow cytometry, proliferative response against mitogens and allogeneic lymphocytes, cytolytic cell activity, and IL-2 production. Antibody-mediated immunocompetence was checked using sheep red blood cell (SRBC)-challenged animals by plaque-forming cell assay and enzyme-linked immunosorbent assay. The dose of AFB1 for the immunosuppressive effects on blastogenic response, IL-2 production, and primary antibody production of splenic cells was much higher than previous studies involving other mice strains. AFB1 decreased the amount of circulating anti-SRBC antibody, and the helper-T cell and B cell populations in phenotyping splenic lymphocytes. There were no significant changes in natural killer cell activity, mixed lymphocyte response, hypothalamic biogenic amine concentrations, and corticotropin releasing factor, and of adrenocorticotropic hormone and corticosterone in plasma. Results were confirmed using adrenalectomized mice. The hypothalamic-pituitary-adrenal axis does not appear to have a major role in AFB1-induced immunotoxicity.

Aflatoxin B1↗