摘要:

The influence of various members of the growth and lactogenic hormone family on the immune system is reviewed. A general hypothesis is proposed for growth control in higher animals. It is suggested that immune reactions, which are based on lymphocyte proliferation, obey the general rules of growth control in vertebrate animals. Growth and lactogenic hormones (GLH) are required for the development and function of the immune system and are suggested to deliver the first signal that prepares the cell for proliferation, differentiation and function. This signal has already been designated by others as the competence signal which initiates the cell cycle. Second signals are delivered through the antigen receptor, and/or by some other cell surface receptors (adhesion molecules) and always involve cell-to-cell (‘bridging’) and/or cell-to-matrix interaction. This category of signals is designated as stromal or adherence signals. The lymphocyte adhesion molecules that mediate second signals have evolved form organ- and tissue-specific recognition/regulatory molecules. The antigen receptors have been perfected during evolution from self recognition to specific-antigen recognition. Apart from this exquisitely specific mechanism of immune recognition, there is evidence for other less specific means of recognition by adherence molecules that mediate the activation of the immune system during nonspecific injury and also play a role in the elimination of degenerated and neoplastic cells. Signals delivered through adhesion molecules have the power to commit the cell to a given activity which is executed by the delivery of third signals in the form of soluble cytokines, usually, but not always, by the same cell delivering the second signal(s). The combination of these three groups of signals will ultimately determine whether or not the cell will proliferate, differentiate, maintain function or, perhaps, be committed to apoptosis. Therefore, GLH maintain immunocompetence which enables the immune system to respond to specific antigenic and tissue-derived stimuli in a self-regulated fashion. The adrenocorticotropic hormone-adrenal axis antagonizes the immunostimulatory effect of GLH. This basic pattern of lymphocyte regulation is influenced further by additional hormones, neurotransmitters and neuropeptides, mostly by the modulation of signal delivery. The constant interaction of neuroendocrine and internal immunoregulatory mechanisms assures the fine tuning of the immune system, so that it is able to functiomn homeostasis and harmony with the organism.

ISSN:1021-7401    

DOI:10.1159/000097168

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

The influence of various members of the growth and lactogenic hormone family on the immune system is reviewed. A general hypothesis is proposed for growth control in higher animals. It is suggested that immune reactions, which are based on lymphocyte proliferation, obey the general rules of growth control in vertebrate animals. Growth and lactogenic hormones (GLH) are required for the development and function of the immune system and are suggested to deliver the first signal that prepares the cell for proliferation, differentiation and function. This signal has already been designated by others as the competence signal which initiates the cell cycle. Second signals are delivered through the antigen receptor, and/or by some other cell surface receptors (adhesion molecules) and always involve cell-to-cell (‘bridging’) and/or cell-to-matrix interaction. This category of signals is designated as stromal or adherence signals. The lymphocyte adhesion molecules that mediate second signals have evolved form organ- and tissue-specific recognition/regulatory molecules. The antigen receptors have been perfected during evolution from self recognition to specific-antigen recognition. Apart from this exquisitely specific mechanism of immune recognition, there is evidence for other less specific means of recognition by adherence molecules that mediate the activation of the immune system during nonspecific injury and also play a role in the elimination of degenerated and neoplastic cells. Signals delivered through adhesion molecules have the power to commit the cell to a given activity which is executed by the delivery of third signals in the form of soluble cytokines, usually, but not always, by the same cell delivering the second signal(s). The combination of these three groups of signals will ultimately determine whether or not the cell will proliferate, differentiate, maintain function or, perhaps, be committed to apoptosis. Therefore, GLH maintain immunocompetence which enables the immune system to respond to specific antigenic and tissue-derived stimuli in a self-regulated fashion. The adrenocorticotropic hormone-adrenal axis antagonizes the immunostimulatory effect of GLH. This basic pattern of lymphocyte regulation is influenced further by additional hormones, neurotransmitters and neuropeptides, mostly by the modulation of signal delivery. The constant interaction of neuroendocrine and internal immunoregulatory mechanisms assures the fine tuning of the immune system, so that it is able to functiomn homeostasis and harmony with the organism.

ISSN:1021-7401    

DOI:10.1159/000315049

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

In this minireview we will discuss some evidence suggesting that the immune response is under neuronal regulation. In particular, we will concentrate on the effects that various neuropeptides have on immunity both in vitro and in vivo. Of these,vasoactive intestinal peptide, substance P, somatostatin, and calcitonin gene related peptide will be discussed in detail. In addition, the effects of nerve growth factor on the immune system will be presented. Finally, a possible role for these neuropeptides in various diseases and its clinical relevance will be suggested.

ISSN:1021-7401    

DOI:10.1159/000097169

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

We have characterized the estrous cycle by obtaining vaginal smears, and quantitating estradiol (E), progesterone (P), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) plasma levels at different phases of the estrous cycle in Lewis (LEW/N) and Fischer (F344/N) rats. Comparison of the duration of the component phases of estrous showed LEW/N metestrous to be significantly longer than in F344/N rats while diestrous and estrous were significantly shorter; proestrous was identical. E levels in LEW/N rats were significantly greater than in F344/N rats only in the estrous phase of the cycle. P levels were significantly greater in LEW/N rats in all phases. LH and FSH levels in the two strains did not differ. Elevated E and P levels would be expected to be associated with increased corticosterone through inhibition of the glucocorticoid negative-feedback pathway. The data reported suggest that other modulating factors in corticotropin-releasing-factor synthesis/release could be overriding both the E and P effects upon hypothalamic-pituitary-adrenal axis responsiveness.

ISSN:1021-7401    

DOI:10.1159/000097170

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

The present study deals with the influence of preferential κ-opioid agonist MR 2034 on experimental allergic encephalomyelitis (EAE). For this purpose, 9-week-old male Dark August rats were treated intraperitoneally with 0.2 mg/kg of MR 2034 as follows: (a) from the day of EAE induction until sacrifice; (b) from the day of EAE induction until the appearance of neurological signs, and (c) from the appearance of neurological signs until sacrifice. Repeated injections of MR 2034 given during the whole period of observation produced the most pronounced suppression of EAE clinical signs, histological lesions in the brain and spinal cord, and anti-myelin basic protein antibody production. These results suggest that κ-opioid receptors may be involved in the development of EAE.

ISSN:1021-7401    

DOI:10.1159/000097171

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

Even though it is widely known that interleukin (IL)-1α acts at the local level, it is still uncertain whether IL-1α is secreted into the circulation and acts at distant sites. We have tried to elucidate this by measuring 24-hour levels of total IL-1α in six healthy female volunteers. Subjects had detectable and pulsatile levels of IL-1α throughout the 24-hour period. The integrated 24-hour IL-1α concentration was 2,367 ± 753 min x μg/1 (mean ± SD), and the integrated pulsatile IL-1α concentration was 553 ± 260 (25 ± 10% ot total integrated IL-1α). The mean IL-1α concentration was 1.63 ± 0.53 μg/1, mean pulse frequency/24 h was 12.8 ± 0.8, mean pulse height was 2.31 ± 0.52 ug/1; mean pulse width was 80.4 ± 2.3 min, and mean interpulse interval was 105.3 ± 2.8 min. Total IL-1α levels significantly correlated with those previously reported for IL-2 in the same samples, and IL-1α pulse parameters which are concentration independent were significantly similar to those of IL-2. Furthermore, cross-correlation analysis indicated that in 83% of our subjects (5/6) there was synchronicity of IL-1α and IL-2 levels. IL-1α pulse parameters were in the range reported for hormones which have well-characterized pulsatility, such as growth hormone, luteinizing hormone, follicle-stimulating hormone, cortisol, β-endorphin, and progesterone. Based on these data we speculate that a pulsatile cytokine cascade may exist in the systemic circulation. The presence of pulsatile IL-1α concentrations in the plasma of healthy women throughout the 24-hour period suggests that IL-1α may function as a classical hormone, being secreted into the blood stream and acting at distant sites, possibly as a component of the response to inflammation and to stress. The source of systemic IL-1α remains to be determined. Future studies of IL-1α blood levels should take into consideration these findings that circulating IL-1α levels exhibit pulsatility.

ISSN:1021-7401    

DOI:10.1159/000097172

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

We studied the effect of intravenous injection of lipopolysaccharide (LPS) (30-250 μg) on the release of several anterior pituitary hormones as indicated by changes in their concentrations in plasma. Within 30 min after intravenous injection of LPS there was a dose-related stimulation of ACTH release; prolactin (PRL) release was induced only by the highest LPS dose injected (250 μg). Even the lowest dose of LPS (30 μg) decreased plasma growth hormone (GH) by 60 min. Higher doses lowered plasma GH by 30 min, but thyroid-stimulating hormone release was only significantly inhibited by the highest dose of LPS. The action of LPS seems to be primarily exerted on the central nervous system, since incubation of hemipitui-taries with LPS for 3 h in doses ranging from 0.001 to 10 μg/ml had no effect on ACTH release. LPS is thought to induce its effects on hormones either by release of cytokines from immune cells which subsequently induce the hormonal changes or possibly by direct action within the hypothalamus. In this report we demonstrate the immunocytochemical localization of a population of interleukin-1α (IL-1α)-like cells in a region extending from the basal forebrain at the level of the diagonal band of Broca, caudally and dorsally to the dorsolateral preoptic region and the hypothalamus at the level of the paraventricular nucleus. Further caudally, IL-1α-like immunoreactive cells were located in the midportion of the amygdala. Two hours after injection of the 125-μg dose of LPS, the number of these immunoreactive cells was dramatically increased. A population of these IL-1α-like cells was identified as neurons on the basis of their morphology and the presence of neurofibrillary protein within them as determined subsequently by double-label immunocytochemistry with a monoclonal antiserum directed against neurofilament protein. The distribution of these neurons encompasses the distribution of the temperature-sensitive neurons within the preoptic-dorsal hypothalamic region suggesting that these neurons, which appear to synthesize and release more IL-1α in response to LPS, are particularly involved in inducing the elevation of body temperature which follows LPS. They could also be involved in mediating the alterations in hypothalamic releasing and inhibiting hormone discharge, which mediate the pattern of pituitary hormone release induced by LPS, although they are not in the same region as the perikarya of most of the hypothalamic peptide-secreting neurons.

ISSN:1021-7401    

DOI:10.1159/000097173

出版商:S. Karger AG    

年代:1994

数据来源: Karger

摘要:

Expression of muscarinic cholinergic receptors (m-AchR) on thymocytes and lymphocytes supports a hypothesis of direct interaction between autonomic innervation and the immune system. Using a muscarinic antagonist, [3H]quinuclidinyl benzilate ([3H]QNB), we revealed different characteristics of m-AchR expression in lymphocytes isolated from the spleen, peripheral blood or thymus of Wistar rats. To further explore the mechanisms controlling m-AchR expression in lymphocytes we have addressed two questions: (i) whether local brain lesions will affect [3H]QNB binding activity of lymphocytes and (ii) whether different antigens will alter m-AchR expression in lymphocytes. We report here that electrolytic lesions of the area hypothalamica anterior resulted in a significant increase in [3H]QNB-specific binding in thymocytes 7 days after neurosurgery. In contrast, local lesions of other hypothalamic structures (area preoptica medialis, area hypothalamica posterior) or sensomotor cortex did not affect m-AchR expression in thymocytes. No apparent changes of [3H]QNB-binding activity were found in lymphocytes isolated from rat spleen or peripheral blood after operation. Both T-cell-dependent (sheep red blood cells) and T-cell-independent (Vi antigen of Salmonella typhi) antigens induced a significant increase in [3H]QNB-specific binding in spleen lymphocytes while [3H]QNB-binding activity of peripheral blood lymphocytes did not change. A different pattern of lymphocyte m-AchR expression found in various lymphoid tissues after immunization or brain lesions suggests a local involvement of cholinergic mechanisms in neuroimmune interaction.

ISSN:1021-7401    

DOI:10.1159/000097174

出版商:S. Karger AG    

年代:1994

数据来源: Karger