Human neutrophil and macrophage chemokinesis induced by cardiopulmonary bypass: Loss of DAME and IL-1 chemotaxis

Stefano, George B.; Bilfinger, Thomas V.

doi:10.1016/0165-5728(93)90029-x

Cited by 39 publications

(21 citation statements)

References 25 publications

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“…The analysis of chemotaxis was determined as noted extensively elsewhere [9,10,15]. Briefly, cells were placed at the extreme right of a petroleum jelly ring in saline in 100-l volumes on a slide, and then covered with a glass cover slip.…”

Section: Analysis Of Cellular Activitymentioning

confidence: 99%

Cell behavior and signal molecule involvement in a case study of malignant histiocytosis: A negative model of morphine as an immunoregulator

Fricchione¹,

Cytryn²,

Bilfinger³

et al. 1997

Am. J. Hematol.

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In a patient diagnosed with histiocytic medullary reticulosis (HM), we examined immunocytes for their responsiveness towards known signaling molecules. Both the granulocytes and monocytes were found to exhibit a high level of spontaneous activation (96% compared to normal cells 7%; P < 0.001). These cells could not be downregulated when exposed to morphine. Following patient treatment with doxorubicin and cyclophosphamide, the immunocytes still exhibited a high spontaneous activation. They responded to morphine exposure in vitro with a cell rounding and becoming immobile for only 20 min whereas normal cells would remain round and immobile for up to 1-2 h. An examination of the plasma from the HM patient revealed that monocyte colony stimulating factor (MCSF) levels were elevated (6.4 and 5.78 compared to a control range of 1-1.75 ng/ml). In the HM patient, the immunocytes did not express the opiate selective and opioid peptide insensitive receptor, mu3, supporting the lack of opiate action. Given this finding, we incubated normal monocytes with MCSF and found that it significantly reduced the mu3 Bmax. Given the role of intracellular calcium in the activation process of immunocytes, we examined the action of various calcium channel blockers for their ability to inhibit the activated HM monocytes. The agents (nimodipine, cardiazem, and verapamil; 10[-9] M) were able to inhibit the HM-associated chemokinesis. Taken together, the data indicate that in the HM patient the immunocytes appear to be overactivated because stimulatory molecules are high and have the ability to downregulate the normal "braking" process. Additionally, the data indicate that MCSF deregulation may be involved as an initiating factor for this disorder.

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Section: Analysis Of Cellular Activitymentioning

confidence: 99%

Cell behavior and signal molecule involvement in a case study of malignant histiocytosis: A negative model of morphine as an immunoregulator

Fricchione¹,

Cytryn²,

Bilfinger³

et al. 1997

Am. J. Hematol.

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“…Monocytes exhibiting a chemotactic response have increased cellular velocity and a parallel alignment to the concentration gradient of the chemotactic agent, whereas, in contrast, a chemokinetic response has no increase in alignment to the stimulating agent. The axis of movement of individual cells is measured where the axis is defined as the minimum moment, or location in a cell, that exhibits minimum rotation around a point and is calculated from the arc tangent of multiple moments, including the centroid location of a cell (30). In previous studies, ϳ30 -40% of monocytes were found to align themselves in a parallel manner with the concentration gradient of known chemotactic agents (30).…”

Section: Monocyte Activation and Chemotaxismentioning

confidence: 99%

“…The lower the number, the higher the perimeter and the more amoeboid the cellular shape. The degree of cellular activation was determined as noted elsewhere (26,29,30). Briefly, under phase contrast optics, round cells appear light yellow and amoeboid cells dark.…”

Section: Monocyte Activation and Chemotaxismentioning

confidence: 99%

“…The axis of movement of individual cells is measured where the axis is defined as the minimum moment, or location in a cell, that exhibits minimum rotation around a point and is calculated from the arc tangent of multiple moments, including the centroid location of a cell (30). In previous studies, ϳ30 -40% of monocytes were found to align themselves in a parallel manner with the concentration gradient of known chemotactic agents (30). Approximately 30 -40 activated cells were observed per 400-m viewing area, and four areas were observed per slide.…”

Section: Monocyte Activation and Chemotaxismentioning

confidence: 99%

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Rebound from Nitric Oxide Inhibition Triggers Enhanced Monocyte Activation and Chemotaxis

Magazine

Chang

Goumon

et al. 2000

The Journal of Immunology

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Exposure of human peripheral blood monocytes to the NO donor S-nitroso-N-acetyl-dl-penicillamine (SNAP) resulted in a rapid shift in cellular conformation of spontaneously activated cells from ameboid to round. The population of activated cells, ∼7.1 ± 1.2%, was reduced 7-fold to 1.1 ± 0.4% following 0.5 h exposure to SNAP. Observation of monocytes for 6 h demonstrated a gradual release from NO inhibition initiating at 2.5 h following SNAP treatment and a period of hyperactivity that was maximal at ∼5 h following SNAP exposure. During the rebound from the NO inhibition phase, there was a significant increase in the population of activated monocytes and an increased responsiveness to chemotactic agents such as IL-1, IL-8, and fMLP relative to that of cells treated with the chemotactic agents alone. Conformational changes induced by SNAP were associated with a reduction in F-actin and loss of filopodial extension. The loss and recovery of F-actin staining paralleled changes in cell activity, suggesting that NO may alter cellular activity by modulation of cytoskeletal actin. These data taken together suggest that inhibition of monocyte activity by NO results in an excitatory phase observed subsequent to release from NO inhibition and increased sensitivity to chemotactic agents. We propose that this rebound from NO inhibition may provide increased immunosurveillance to rectify immunological problems that have been encountered during the period of inhibition.

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“…Additional information on opiate alkaloid signaling substances can be summarized as follows: Injection of vertebrate animals with morphine results in deficient macrophage function [106] and an alteration of T-cell activity [107]. Morphine also antagonizes interleukin-1alpha or tumor necrosis factor-alpha-induced chemotaxis in human granulocytes and monocytes [108,109]. …”

mentioning

confidence: 99%

Endogenous morphine/nitric oxide-coupled regulation of cellular physiology and gene expression: Implications for cancer biology

Stefano

Kream

Mantione

et al. 2008

Seminars in Cancer Biology

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Cancer is a simplistic, yet complicated, process that promotes uncontrolled growth. In this regard, this unconstrained proliferation may represent primitive phenomena whereby cellular regulation is suspended or compromised. Given the new empirical evidence for a morphinergic presence and its profound modulatory actions on several cellular processes it is not an overstatement to hypothesize that morphine may represent a key chemical messenger in the process of modulating proliferation of diverse cells. This has been recently demonstrated by the finding of a novel opiate-alkaloid selective receptor subtype in human multilineage progenitor cells (MLPC). Adding to the significance of morphinergic signaling are the findings of its presence in plant, invertebrate and vertebrate cells, which also have been shown to synthesize this messenger as well. Interestingly, we and others have shown that some cancerous tissues contain morphine. Furthermore, in medullary histolytic reticulosis, which is exemplified by cells having hyperactivity, the mu3 (μ 3 ) opiate select receptor was not present. Thus, it would appear that morphinergic signaling has inserted itself in many processes taking a long time to evolve, including those regulating the proliferation of cells across diverse phyla.Keywords endogenous morphine; μ 3 opiate receptor; nitric oxide; stem cell; cancer * Corresponding Author: Dr. George B. Stefano, Neuroscience Research Institute, SUNY College at Old Westbury, P.O. Box 210, Old Westbury, NY 11568, USA Tel: 001-516-876-2732; Fax: 001-516-876-2727; Email: gstefano@sunynri.org. Email addresses: gstefano@sunynri.org (GB Stefano); rmkream@sunynri.org (RM Kream); kmantione@sunynri.org (KJ Mantione); msheehan@sunynri.org (M Sheehan); patcad@sunynri.org (P Cadet); zhuwei@sunynri.org (W Zhu); tbilfinger@notes.cc.sunysb.edu (TV Bilfinger); esch@fh-coburg.de (T Esch) Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptSemin Cancer Biol. Author manuscript; available in PMC 2009 June 1. Historical Context and Clinical ImplicationsMorphine and chemically related opiate alkaloids represent time-tested analgesic principles for management of severe pain associated with metastatic disease [1,2]. A substantial body of accumulated evidence, however, documents a cadre of cellular/physiological effects associated with pharmacological administration of morphine and related opiate alkaloids that lie outside the realm of anti-nociception and appear to be mediated by indirect and/or "non-traditional" mechanisms. Notably, complementary studies have monitored ...

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Human neutrophil and macrophage chemokinesis induced by cardiopulmonary bypass: Loss of DAME and IL-1 chemotaxis

Cited by 39 publications

References 25 publications

Cell behavior and signal molecule involvement in a case study of malignant histiocytosis: A negative model of morphine as an immunoregulator

Cell behavior and signal molecule involvement in a case study of malignant histiocytosis: A negative model of morphine as an immunoregulator

Rebound from Nitric Oxide Inhibition Triggers Enhanced Monocyte Activation and Chemotaxis

Endogenous morphine/nitric oxide-coupled regulation of cellular physiology and gene expression: Implications for cancer biology

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