摘要:

In vivo and in vitro data combined show that prolactin (PRL) can mimic or interact with known lymphocyte cytokines and that these, in turn, can regulate PRL synthesis at the site of immune response. In contrast, pituitary PRL is under the control of both immune system products (non-cognitive stimuli) and signals to the CNS (cognitive stimuli). The role of PRL as a cytokine and as an endocrine hormone is discussed. In particular, assignment of PRL to the T helper 1 phenotype is proposed, based on its ability to enhance NK cell function, activate the interferon-regulated factor (IRF-1) transcription factor and to interact with or generate IL-2 and IFNy. Since hyperprolactinemia and hypoprolactinemia are both immunosuppressive, physiological levels of circulating PRL must be necessary to maintain normal immunocompetence. Moderate increases in PRL during immune stimulation of the hypothalamic-pituitary axis may counteract glucocorticoid inhibition, whereas inappropriate prolongation of PRL synthesis could lead to autoimmune diseases. Increased release of PRL by the pituitary during stress may inhibit NK cell antitumor cytotoxicity. The variety of PRL isotypes, the existence of multiple receptor subunits, and the complexity of their intracellular signaling may explain the specificity of PRL action on different target cells.

ISSN:1021-7401    

DOI:10.1159/000097335

出版商:S. Karger AG    

年代:1997

数据来源: Karger

摘要:

The serum antibody response to ovalbumin (OA) has been investigated following intracerebroventricular (i.c.v.) and intravenous administration of antigen in the rat, under altered neuronal and immunological conditions. I.c.v. administration of antigen was far more potent in eliciting humoral immune response. Central nervous system (CNS) immunization under the conditions of disrupted blood-brain barrier decreased anti-OA antibody production. Peripheral polyclonal stimulation with Bordetella pertussis increased production of specific antibodies to i.c.v. injected antigen, while complete Freund's adjuvant had no effect on the immune response. These results suggest that CNS compartmentalization of antigen may be critical for mounting strong antibody production, and that peripheral polyclonal stimulation of the immune system may markedly contribute to the overall intensity of the immune response.

ISSN:1021-7401    

DOI:10.1159/000097336

出版商:S. Karger AG    

年代:1997

数据来源: Karger

摘要:

We have investigated the role of circulating glucocorticoids in the suppression of the hypothalamic-pituitary-thyroid (HPT) axis following lipopolysaccharide (LPS) injection in rats. Intraperitoneal injection of LPS (2.5 mg/kg) suppressed paraventricular nucleus thyrotropin-releasing hormone (TRH) mRNA, pituitary thyroid-stimulating hormone (TSH) mRNA and plasma triiodothyronine. In these animals LPS also increased paraventricular nucleus corticotropin-releasing hormone (CRH) mRNA, pituitary proopiomelanocortin (POMC) mRNA and plasma corticosterone levels. To investigate the role of plasma corticosterone in the suppression of the HPT axis, we clamped the plasma corticosterone level at morning baseline level by bilateral adrenalectomy and corticosterone pellet implantation. Ten days after surgery, LPS injection evoked a dramatic increase in CRH mRNA and POMC mRNA. Despite the lack of change in plasma corticosterone in the corticosterone-clamped rats, LPS was still able to suppress TRH and TSH mRNA levels in both corticosterone-clamped and sham-operated rats. These data indicate that in response to LPS, suppression of the HPT axis occurs and is independent of the LPS-induced increase in plasma corticosterone.

ISSN:1021-7401    

DOI:10.1159/000097337

出版商:S. Karger AG    

年代:1997

数据来源: Karger

摘要:

Neuronal mortality, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNFα) release were measured in hypoxic hippocampal neuronal cultures. Release of IL1β and TNFα was already observed in normoxic cultures, but after hypoxia it was increased approximately 2-fold. Pretreatment with 2-amino-5-phosphonovaleric acid (APV), the N-methyl-D-aspartate (NMDA) receptor antagonist, not only decreased neuronal mortality as expected, but also dramatically lowered cytokine release. However, there was no relationship between the neuronal mortality and the release of each cytokine both in untreated hypoxic cultures and in APV-pretreated ones. We conclude that IL1β and TNFα release in hypoxia are dependent on the activation of the NMDA receptor, but that this is not the main mechanism of hypoxia damage in in vitro neuronal cultures.

ISSN:1021-7401    

DOI:10.1159/000097338

出版商:S. Karger AG    

年代:1997

数据来源: Karger

ISSN:1021-7401    

DOI:10.1159/000097339

出版商:S. Karger AG    

年代:1997

数据来源: Karger

ISSN:1021-7401    

DOI:10.1159/000315351

出版商:S. Karger AG    

年代:1997

数据来源: Karger