Coordinated host defense through an integration of the neural, immune and haemopoietic systems

Miyan, Jaleel; Broome, Caroline S.; Afan, A. M.

doi:10.1016/s0739-7240(98)00033-2

Cited by 27 publications

(14 citation statements)

References 15 publications

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“…Because SP is a hemopoietic stimulator, it is logical to assume that this report showing a link between SP-SDF-1␣-hemopoietic axis could be linked to the nervous system. Evidence has shown that often the signal to increase hemopoiesis comes from the central nervous system and is regulated secondarily by cytokines (23,24). For example, the SDF-1␣ shown in this report could be a mediator in the neural-hemopoietic response through SP and perhaps other neurotransmitters.…”

Section: Discussionmentioning

confidence: 62%

Stromal Derived Growth Factor-1α: Another Mediator in Neural-Emerging Immune System through Tac1 Expression in Bone Marrow Stromal Cells

Corcoran¹,

Patel²,

Rameshwar

2007

The Journal of Immunology

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Stromal cell-derived growth factor-1α (SDF-1α) is a member of the CXC chemokines and interacts with the G protein, seven-transmembrane CXCR4 receptor. SDF-1α acts as a chemoattractant for immune and hemopoietic cells. The Tac1 gene encodes peptides belonging to the tachykinin family with substance P being the predominant member. Both SDF-1α and Tac1 peptides are relevant hemopoietic regulators. This study investigated the effects of SDF-1α on Tac1 expression in the major hemopoietic supporting cells, the bone marrow stroma, and addresses the consequence to hemopoiesis. Reporter gene assays with the 5′ flanking region of Tac1 showed a bell-shaped effect of SDF-1α on luciferase activity with 20 ng/ml SDF-1α acting as stimulator, whereas 50 and 100 ng/ml SDF-1α acted as inhibitors. Gel shift assays and transfection with wild-type and mutant IκB indicate NF-κB as a mediator in the repressive effects at 50 and 100 ng/ml SDF-1α. Northern analyses and ELISA showed correlations among reporter gene activities, mRNA (β-preprotachykinin I), and protein levels for substance P. Of relevance is the novel finding by long-term culture-initiating cell assays that showed an indirect effect of SDF-1α on hemopoiesis through substance P production. The results also showed neurokinin 1 and not neurokinin 2 as the relevant receptor. Another crucial finding is that substance P does not regulate the production of SDF-1α in stroma. The studies indicate that SDF-1α levels above baseline production in bone marrow stroma induce the production of substance P to stimulate hemopoiesis. Substance P, however, does not act as autocrine stimulator to induce the production of SDF-1α. This study adds SDF-1α as a mediator within the neural-immune-hemopoietic axis.

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Section: Discussionmentioning

confidence: 62%

Stromal Derived Growth Factor-1α: Another Mediator in Neural-Emerging Immune System through Tac1 Expression in Bone Marrow Stromal Cells

Corcoran¹,

Patel²,

Rameshwar

2007

The Journal of Immunology

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“…[23,24] As stromal cells are vital to regulation of hematopoiesis, their neural control has been suggested to be involved in this homeostatic function. In this respect, published data indicate that neuropeptides influence the proliferation and/or rate of maturation of myeloid progenitor cells probably through a local effect on stromal cells.…”

Section: Discussionmentioning

confidence: 99%

Myelopoietic Response in Mice Exposed to Acute Cold/Restraint Stress: Modulation by Chlorella vulgaris Prophylactic Treatment

Queiroz

Malacrida

Justo

et al. 2004

Immunopharmacology and Immunotoxicology

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In this study, hematopoietic cells from mice pretreated with CVE and exposed to acute cold/restraint stress were stimulated in the presence of growth factors to form colonies, thus providing accurate information about the modulation of the green algae of the stress-induced changes in the hematopoietic response. Our results demonstrated that exposure to acute stress affected hematopoiesis. Mice exposed for a 2.5-hour time period of cold and restraint presented diminished clonal capacity for CFU-GM content per femur, which was decreased by as much as 50% compared with that in control mice, in spite of the significant increase in serum colony-stimulating activity (CSA). Treatment with 50 mg/kg CVE for 5 days, previously to the stress regimen, attenuates the effects of the stress, since comparable levels of myeloid progenitors were found in the bone marrow of both CVE/stress and control mice. Moreover, the sera from stressed mice pretreated with CVE further increased the CFU-GM formation. On the contrary, the spleen seemed to be less sensitive to acute stress in our experimental conditions. These findings are in line with our previous reports showing that the stress-induced reduction in bone marrow CFU-GM of rats exposed to electric shocks is mediated by activation of the HPA axis and by secretion of opioid agonists. No changes were observed in bone marrow, spleen and thymus total cell counts, and in relative organ weights. However, a 50% reduction in the body weight loss produced by the stress was observed in mice given the extract.

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“…12 Indeed, there is a bi-directional communication between the brain and the immune system, such that alterations in one can lead to profound changes in the other, during development as well as in maturity. 13,14 In this review, we first summarize relevant pathological and molecular findings for schizophrenia and correlate them with abnormalities found in the neurotrophic factor/cytokine systems thus far. We draw attention to the roles of growth factors and cytokines in regulating brain development, and particularly the control of those proteins that are known to be altered in schizophrenia.…”

Section: Nutritionalmentioning

confidence: 99%

Cytokine and growth factor involvement in schizophrenia—support for the developmental model

2000

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Medical treatment with various cytokines can provoke psychiatric symptoms. Conversely, psychiatric patients can display abnormalities in cytokine and neurotrophic factor expression. Such observations have pointed to the potential contribution of cytokines and growth factors to schizophrenic pathology and/or etiology. The cellular targets of the relevant factors and the nature of their actions remain to be explored in mental illness, however. Recent physiological studies demonstrate that cytokines and neurotrophic factors can markedly influence synaptic transmission and plasticity upon acute or chronic application. Moreover, many of the molecular alterations observed in the schizophrenic brain are consistent with abnormalities in cytokine and neurotrophic factor regulation of these molecules. In this review, we summarize these molecular pathology findings for schizophrenia and highlight the neurodevelopmental activities of cytokines and neurotrophic factors that may contribute to the etiology or pathology of this illness. Molecular Psychiatry (2000) 5, 594-603.

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Coordinated host defense through an integration of the neural, immune and haemopoietic systems

Cited by 27 publications

References 15 publications

Stromal Derived Growth Factor-1α: Another Mediator in Neural-Emerging Immune System through Tac1 Expression in Bone Marrow Stromal Cells

Stromal Derived Growth Factor-1α: Another Mediator in Neural-Emerging Immune System through Tac1 Expression in Bone Marrow Stromal Cells

Myelopoietic Response in Mice Exposed to Acute Cold/Restraint Stress: Modulation by Chlorella vulgaris Prophylactic Treatment

Cytokine and growth factor involvement in schizophrenia—support for the developmental model

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