1
40
11
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Text
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<a href="http://doi.org/10.1016/j.npep.2007.06.001" target="_blank" rel="noreferrer">http://doi.org/10.1016/j.npep.2007.06.001</a>
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Title
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Targeting of opioid-producing leukocytes for pain control
Publisher
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Neuropeptides
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
Subject
The topic of the resource
Biomarkers of Pain
Creator
An entity primarily responsible for making the resource
Machelska H
Description
An account of the resource
It is accepted that inflammatory mediators released from leukocytes contribute to the generation of pain. However, it is less well known that immune cells also produce mediators that can effectively counteract pain. These include anti-inflammatory cytokines and opioid peptides. This article concentrates on recent evidence that interactions between leukocyte-derived opioid peptides and their receptors on peripheral sensory neurons can result in potent, clinically relevant inhibition of pathological pain. Inflammation of peripheral tissues leads to increased synthesis and axonal transport of opioid receptors in dorsal root ganglion neurons. This results in opioid receptor upregulation and enhanced G-protein coupling at peripheral sensory nerve terminals. These events are dependent on neuronal electrical activity, production of proinflammatory cytokines and nerve growth factor within the inflamed tissue. Together with the disruption of the perineurial barrier, all these changes lead to an enhanced peripheral analgesic efficacy of opioids. The major source of local endogenous opioid ligands (beta-endorphin, enkephalins, endomorphins and dynorphin) are leukocytes. These cells contain and upregulate signal-sequence encoding mRNA of the beta-endorphin precursor proopiomelanocortin and the entire enzymatic machinery necessary for its processing into the functionally active peptide. Opioid-containing immune cells extravasate using adhesion molecules and chemokines to accumulate in inflamed tissues. Upon stressful stimuli or in response to releasing agents such as corticotropin-releasing factor, cytokines, chemokines and catecholamines, leukocytes secrete opioids. Depending on the cell type, this release is contingent on extracellular Ca(2+) or on inositol triphosphate receptor-triggered release of Ca(2+) from endoplasmic reticulum. Once secreted opioid peptides activate peripheral opioid receptors and produce analgesia by inhibiting the excitability of sensory nerves and/or the release of excitatory neuropeptides. These effects occur without central untoward side effects such as depression of breathing, clouding of consciousness or addiction. Future aims include the selective targeting of opioid-containing leukocytes to sites of painful injury and the augmentation of opioid peptide and receptor synthesis.
2007
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.npep.2007.06.001" target="_blank" rel="noreferrer">10.1016/j.npep.2007.06.001</a>
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Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2007
Backlog
Biomarkers of Pain
Journal Article
Machelska H
Neuropeptides
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1189/jlb.0405223" target="_blank" rel="noreferrer">http://doi.org/10.1189/jlb.0405223</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Leukocytes in the regulation of pain and analgesia
Publisher
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Journal Of Leukocyte Biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
Subject
The topic of the resource
Humans; Analgesia; Animals; Biomarkers of Pain; Receptors; Biomarkers Reference List; Pain/immunology/physiopathology; Inflammation Mediators/immunology; Leukocytes/immunology/secretion; Nervous System/immunology/physiopathology; Neuropeptides/immunology/pharmacology; Opioid Peptides/immunology/secretion; Opioid/immunology; Sensory/immunology/physiopathology; Signal Transduction/immunology
Creator
An entity primarily responsible for making the resource
Rittner HL; Machelska H; Stein C
Description
An account of the resource
When tissue is destroyed or invaded by leukocytes in inflammation, numerous mediators are delivered by the circulation and/or liberated from resident and immigrated cells at the site. Proalgesic mediators include proinflammatory cytokines, chemokines, protons, nerve growth factor, and prostaglandins, which are produced by invading leukocytes or by resident cells. Less well known is that analgesic mediators, which counteract pain, are also produced in inflamed tissues. These include anti-inflammatory cytokines and opioid peptides. Interactions between leukocyte-derived opioid peptides and opioid receptors can lead to potent, clinically relevant inhibition of pain (analgesia). Opioid receptors are present on peripheral endings of sensory neurons. Opioid peptides are synthesized in circulating leukocytes, which migrate to inflamed tissues directed by chemokines and adhesion molecules. Under stressful conditions or in response to releasing agents (e.g., corticotropin-releasing factor, cytokines, noradrenaline), leukocytes can secrete opioids. They activate peripheral opioid receptors and produce analgesia by inhibiting the excitability of sensory nerves and/or the release of excitatory neuropeptides. This review presents discoveries that led to the concepts of pain generation by mediators secreted from leukocytes and of analgesia by immune-derived opioids.
2005
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1189/jlb.0405223" target="_blank" rel="noreferrer">10.1189/jlb.0405223</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2005
Analgesia
Animals
Backlog
Biomarkers of Pain
Biomarkers Reference List
Humans
Inflammation Mediators/immunology
Journal Article
Journal Of Leukocyte Biology
Leukocytes/immunology/secretion
Machelska H
Nervous System/immunology/physiopathology
Neuropeptides/immunology/pharmacology
Opioid Peptides/immunology/secretion
Opioid/immunology
Pain/immunology/physiopathology
Receptors
Rittner HL
Sensory/immunology/physiopathology
Signal Transduction/immunology
Stein C
-
Text
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Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/j.pain.2004.08.029" target="_blank" rel="noreferrer">http://doi.org/10.1016/j.pain.2004.08.029</a>
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Title
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Control of inflammatory pain by chemokine-mediated recruitment of opioid-containing polymorphonuclear cells
Publisher
An entity responsible for making the resource available
Pain
Date
A point or period of time associated with an event in the lifecycle of the resource
2004
Subject
The topic of the resource
Male; Pain Measurement; Analysis of Variance; Animals; Rats; Non-U.S. Gov't; Research Support; Comparative Study; Dose-Response Relationship; Drug; Receptors; Naloxone/pharmacology; Freund's Adjuvant; Wistar; Flow Cytometry/methods; Antibodies/pharmacology; Cell Count/methods; Cell Movement/physiology; Chemokines; Chemokines/immunology/physiology; Corticotropin-Releasing Hormone/therapeutic use; CXC/immunology/metabolism; Drug Administration Routes; Enzyme-Linked Immunosorbent Assay/methods; Gene Expression Regulation/physiology; Immunohistochemistry/methods; Intercellular Signaling Peptides and Proteins/immunology/metabolism; Interleukin-8B/metabolism; Narcotics/metabolism; Neurogenic Inflammation/chemically induced/complications/therapy; Neutrophils/metabolism; Pain Threshold/drug effects; Pain/etiology/therapy
Creator
An entity primarily responsible for making the resource
Brack A; Rittner HL; Machelska H; Leder K; Mousa SA; Schafer M; Stein C
Description
An account of the resource
Opioid-containing leukocytes can counteract inflammatory hyperalgesia. Under stress or after local injection of corticotropin releasing factor (CRF), opioid peptides are released from leukocytes, bind to opioid receptors on peripheral sensory neurons and mediate antinociception. Since polymorphonuclear cells (PMN) are the predominant opioid-containing leukocyte subpopulation in early inflammation, we hypothesized that PMN and their recruitment by chemokines are important for peripheral opioid-mediated antinociception at this stage. Rats were intraplantarly injected with complete Freund's adjuvant (CFA). Using flow cytometry, immunohistochemistry, and ELISA, leukocyte subpopulations, chemokine receptor (CXCR2) expression on opioid-containing leukocytes and the CXCR2 ligands keratinocyte-derived chemokine (KC), macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant-2 (CINC-2) were quantified. Paw pressure threshold (PPT) was determined before and after intraplantar and subcutaneous injection of CRF with or without naloxone. PMN depletion was achieved by intravenous injection of an antiserum. Chemokines were blocked by intraplantar injection of anti-MIP-2 and/or anti-KC antiserum. We found that at 2 h post CFA (i) intraplantar but not subcutaneous injection of CRF produced dose-dependent and naloxone-reversible antinociception (P0.05, ANOVA). In summary, in early inflammation peripheral opioid-mediated antinociception is critically dependent on PMN and their recruitment by CXCR2 chemokines.
2004
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.pain.2004.08.029" target="_blank" rel="noreferrer">10.1016/j.pain.2004.08.029</a>
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Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2004
Analysis of Variance
Animals
Antibodies/pharmacology
Backlog
Brack A
Cell Count/methods
Cell Movement/physiology
Chemokines
Chemokines/immunology/physiology
Comparative Study
Corticotropin-Releasing Hormone/therapeutic use
CXC/immunology/metabolism
Dose-Response Relationship
Drug
Drug Administration Routes
Enzyme-Linked Immunosorbent Assay/methods
Flow Cytometry/methods
Freund's Adjuvant
Gene Expression Regulation/physiology
Immunohistochemistry/methods
Intercellular Signaling Peptides and Proteins/immunology/metabolism
Interleukin-8B/metabolism
Journal Article
Leder K
Machelska H
Male
Mousa SA
Naloxone/pharmacology
Narcotics/metabolism
Neurogenic Inflammation/chemically induced/complications/therapy
Neutrophils/metabolism
Non-U.S. Gov't
Pain
Pain Measurement
Pain Threshold/drug effects
Pain/etiology/therapy
Rats
Receptors
Research Support
Rittner HL
Schafer M
Stein C
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/s0165-5728(02)00049-8" target="_blank" rel="noreferrer">http://doi.org/10.1016/s0165-5728(02)00049-8</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Immunohistochemical localization of endomorphin-1 and endomorphin-2 in immune cells and spinal cord in a model of inflammatory pain
Publisher
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Journal Of Neuroimmunology
Date
A point or period of time associated with an event in the lifecycle of the resource
2002
Subject
The topic of the resource
Male; Animals; Rats; Biomarkers of Pain; Immunohistochemistry; Freund's Adjuvant; Hindlimb; Wistar; Lymph Nodes/cytology; Lymphocytes/chemistry; Macrophages/chemistry; Monocytes/chemistry; Oligopeptides/analysis; Pain/chemically induced/immunology; Posterior Horn Cells/chemistry; Skin/chemistry/immunology/innervation
Creator
An entity primarily responsible for making the resource
Mousa SA; Machelska H; Schafer M; Stein C
Description
An account of the resource
Recently, two novel highly selective mu-opioid receptor (MOR) agonists, endomorphin-1 and endomorphin-2, have been isolated from bovine as well as human brains and were proposed to be the endogenous ligand for MOR. Later, endomorphin-1 and endomorphin-2 have been detected in the immune system of rats and humans using radioimmunoassay in combination with reverse-high-phase-liquid chromatography. In the present study, we analyzed the expression of endomorphin-1, endomorphin-2 and MOR by immunohistochemistry in a model of Freund's complete adjuvant (FCA)-induced painful inflammation. While MOR was upregulated on peripheral and central nerve terminals, inflammation did not alter endomorphin-2 expression in nerve fibers either in the dorsal horn of the spinal cord or in subcutaneous tissue. Endomorphin-1 and endomorphin-2 were expressed in immune cells (macrophage/monocytes) in the medullary region of the popliteal lymph nodes. The proportion of immunocytes (macrophage/monocytes, lymphocytes) containing endomorphin-1 and endomorphin-2 was increased in inflamed lymph nodes and subcutaneous paw tissue of animals with local inflammatory pain. Taken together, the upregulation of MOR and of its endogenous ligands endomorphin-1 and endomorphin-2 in immunocytes suggests an involvement of these opioid peptides in the peripheral control of inflammatory pain.
2002
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/s0165-5728(02)00049-8" target="_blank" rel="noreferrer">10.1016/s0165-5728(02)00049-8</a>
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Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2002
Animals
Backlog
Biomarkers of Pain
Freund's Adjuvant
Hindlimb
Immunohistochemistry
Journal Article
Journal Of Neuroimmunology
Lymph Nodes/cytology
Lymphocytes/chemistry
Machelska H
Macrophages/chemistry
Male
Monocytes/chemistry
Mousa SA
Oligopeptides/analysis
Pain/chemically induced/immunology
Posterior Horn Cells/chemistry
Rats
Schafer M
Skin/chemistry/immunology/innervation
Stein C
Wistar
-
Text
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Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/s0165-5728(03)00213-3" target="_blank" rel="noreferrer">http://doi.org/10.1016/s0165-5728(03)00213-3</a>
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The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Different mechanisms of intrinsic pain inhibition in early and late inflammation
Publisher
An entity responsible for making the resource available
Journal Of Neuroimmunology
Date
A point or period of time associated with an event in the lifecycle of the resource
2003
Subject
The topic of the resource
Male; Time Factors; Pain Threshold; Animals; Rats; Biomarkers of Pain; Injections; Subcutaneous; Enkephalin; Hindlimb; Wistar; Corticotropin-Releasing Hormone/administration & dosage; Dynorphins/antagonists & inhibitors/biosynthesis/physiology; Edema/immunology/metabolism/physiopathology; Endorphins/antagonists & inhibitors/biosynthesis/physiology; Freund's Adjuvant/administration & dosage; Inflammation/immunology/metabolism/physiopathology; Leukocytes/drug effects/metabolism/physiology; Methionine/antagonists & inhibitors/biosynthesis/physiology; Naloxone/administration & dosage; Pain/immunology/pathology/prevention & control; Stress/immunology/metabolism/physiopathology
Creator
An entity primarily responsible for making the resource
Machelska H; Schopohl JK; Mousa SA; Labuz D; Schafer M; Stein C
Description
An account of the resource
Neuroimmune interactions control pain through activation of opioid receptors on sensory nerves by immune-derived opioid peptides. Here we evaluate mechanisms of intrinsic pain inhibition at different stages of Freund's adjuvant-induced inflammation of the rat paw. We use immunohistochemistry and paw pressure testing. Our data show that in early (6 h) inflammation leukocyte-derived beta-endorphin, met-enkephalin and dynorphin A activate peripheral mu-, delta- and kappa-receptors to inhibit nociception. In addition, central opioid mechanisms seem to contribute significantly to this effect. At later stages (4 days), antinociception is exclusively produced by leukocyte-derived beta-endorphin acting at peripheral mu and delta receptors. Corticotropin-releasing hormone (CRH) is an endogenous trigger of these effects at both stages. These findings indicate that peripheral opioid mechanisms of pain inhibition gain functional relevance with the chronicity of inflammation.
2003
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/s0165-5728(03)00213-3" target="_blank" rel="noreferrer">10.1016/s0165-5728(03)00213-3</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2003
Animals
Backlog
Biomarkers of Pain
Corticotropin-Releasing Hormone/administration & dosage
Dynorphins/antagonists & inhibitors/biosynthesis/physiology
Edema/immunology/metabolism/physiopathology
Endorphins/antagonists & inhibitors/biosynthesis/physiology
Enkephalin
Freund's Adjuvant/administration & dosage
Hindlimb
Inflammation/immunology/metabolism/physiopathology
Injections
Journal Article
Journal Of Neuroimmunology
Labuz D
Leukocytes/drug effects/metabolism/physiology
Machelska H
Male
Methionine/antagonists & inhibitors/biosynthesis/physiology
Mousa SA
Naloxone/administration & dosage
Pain Threshold
Pain/immunology/pathology/prevention & control
Rats
Schafer M
Schopohl JK
Stein C
Stress/immunology/metabolism/physiopathology
Subcutaneous
Time Factors
Wistar
-
Text
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Backlog
URL Address
<a href="http://doi.org/10.1038/nm908" target="_blank" rel="noreferrer">http://doi.org/10.1038/nm908</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Attacking pain at its source: new perspectives on opioids
Publisher
An entity responsible for making the resource available
Nature Medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2003
Subject
The topic of the resource
Humans; Analgesics; Animals; Non-U.S. Gov't; Research Support; Drug Tolerance; Receptors; Ligands; Afferent/metabolism; Cell Movement; Neurons; Opioid Peptides/metabolism/therapeutic use; Opioid/genetics/metabolism; Opioid/metabolism/therapeutic use; Pain/drug therapy/metabolism/therapy; Signal Transduction/physiology
Creator
An entity primarily responsible for making the resource
Stein C; Schafer M; Machelska H
Description
An account of the resource
The treatment of severe pain with opioids has thus far been limited by their unwanted central side effects. Recent research promises new approaches, including opioid analgesics acting outside the central nervous system, targeting of opioid peptide-containing immune cells to peripheral damaged tissue, and gene transfer to enhance opioid production at sites of injury.
2003
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1038/nm908" target="_blank" rel="noreferrer">10.1038/nm908</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2003
Afferent/metabolism
Analgesics
Animals
Backlog
Cell Movement
Drug Tolerance
Humans
Journal Article
Ligands
Machelska H
Nature Medicine
Neurons
Non-U.S. Gov't
Opioid Peptides/metabolism/therapeutic use
Opioid/genetics/metabolism
Opioid/metabolism/therapeutic use
Pain/drug therapy/metabolism/therapy
Receptors
Research Support
Schafer M
Signal Transduction/physiology
Stein C
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1097/00000542-200401000-00024" target="_blank" rel="noreferrer">http://doi.org/10.1097/00000542-200401000-00024</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Mobilization of opioid-containing polymorphonuclear cells by hematopoietic growth factors and influence on inflammatory pain
Publisher
An entity responsible for making the resource available
Anesthesiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2004
Subject
The topic of the resource
Male; Animals; Rats; Biomarkers of Pain; Inflammation/complications; RNA; Pain Measurement/drug effects; Radioimmunoassay; Pain/drug therapy/physiopathology; Wistar; Neutrophils/metabolism; Messenger/biosynthesis; DNA Primers; Reverse Transcriptase Polymerase Chain Reaction; Flow Cytometry; Cell Adhesion Molecules/pharmacology; Cell Separation; Chemokines/biosynthesis; Chemotaxis; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology; Hindlimb/physiology; Leukocyte/drug effects; Light; Narcotics/metabolism/pharmacology; Stem Cell Factor/pharmacology
Creator
An entity primarily responsible for making the resource
Brack A; Rittner HL; Machelska H; Beschmann K; Sitte N; Schafer M; Stein C
Description
An account of the resource
BACKGROUND: Leukocytes can control inflammatory pain by secretion of opioid peptides, stimulated by cold-water swimming or local injection of corticotropin-releasing factor, and subsequent activation of opioid receptors on peripheral sensory neurons. This study investigated whether mobilization of polymorphonuclear cells (PMN) by granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) enhances immigration of opioid-containing PMN and peripheral opioid analgesia in rats with Freund complete adjuvant-induced hind paw inflammation. METHODS: In circulating PMN of rats treated with G-CSF+SCF and sham-treated rats, opioid peptide content was measured by radioimmunoassay. Expression of adhesion molecules (CD62L, CD49d, CD18), in vitro migration in the Boyden chamber, and infiltrating leukocytes were analyzed by flow cytometry. Chemokine messenger RNA transcription was quantified by LightCycler polymerase chain reaction. Paw pressure threshold was measured at baseline, after cold-water swimming, and after injection of corticotropin-releasing factor. RESULTS: G-CSF+SCF treatment increased circulating PMN (11-fold, P 0.05). CONCLUSIONS: G-CSF+SCF mobilized circulating opioid-containing PMN but had a minor influence on cell migration and peripheral analgesia, probably because of the low expression of chemokines in the inflamed paw and one of the decreased beta-endorphin content in PMN.
2004
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/00000542-200401000-00024" target="_blank" rel="noreferrer">10.1097/00000542-200401000-00024</a>
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Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2004
Anesthesiology
Animals
Backlog
Beschmann K
Biomarkers of Pain
Brack A
Cell Adhesion Molecules/pharmacology
Cell Separation
Chemokines/biosynthesis
Chemotaxis
DNA Primers
Flow Cytometry
Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology
Hindlimb/physiology
Inflammation/complications
Journal Article
Leukocyte/drug effects
Light
Machelska H
Male
Messenger/biosynthesis
Narcotics/metabolism/pharmacology
Neutrophils/metabolism
Pain Measurement/drug effects
Pain/drug therapy/physiopathology
Radioimmunoassay
Rats
Reverse Transcriptase Polymerase Chain Reaction
Rittner HL
RNA
Schafer M
Sitte N
Stein C
Stem Cell Factor/pharmacology
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1097/00000542-200407000-00031" target="_blank" rel="noreferrer">http://doi.org/10.1097/00000542-200407000-00031</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Tissue monocytes/macrophages in inflammation: hyperalgesia versus opioid-mediated peripheral antinociception
Publisher
An entity responsible for making the resource available
Anesthesiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2004
Subject
The topic of the resource
Male; Analgesics; Animals; Rats; Biomarkers of Pain; Injections; Pain Measurement/drug effects; Freund's Adjuvant; Wistar; Flow Cytometry; Foot/pathology; Opioid/administration & dosage/pharmacology; Clodronic Acid/pharmacokinetics/pharmacology; Fentanyl/administration & dosage/pharmacology; Heat; Hyperalgesia/chemically induced/pathology/psychology; Inflammation/chemically induced/pathology; Liposomes; Macrophages/pathology; Monocytes/pathology; Non-Narcotic/pharmacokinetics/pharmacology; Pressure
Creator
An entity primarily responsible for making the resource
Brack A; Labuz D; Schiltz A; Rittner HL; Machelska H; Schafer M; Reszka R; Stein C
Description
An account of the resource
BACKGROUND: Opioid-containing leukocytes migrate to peripheral sites of inflammation. On exposure to stress, opioid peptides are released, bind to opioid receptors on peripheral sensory neurons, and induce endogenous antinociception. In later stages of Freund's complete adjuvant-induced local inflammation, monocytes/macrophages are a major opioid-containing leukocyte subpopulation, but these cells also produce proalgesic cytokines. In this study, the role of tissue monocytes/macrophages in hyperalgesia and in peripheral opioid-mediated antinociception was investigated. METHODS: After intraplantar injection of Freund's adjuvant, leukocyte subpopulations and opioid-containing leukocytes were analyzed by flow cytometry in the inflamed paw in the presence or absence of monocyte/macrophage depletion by intraplantar injection of clodronate-containing liposomes (phosphate-buffered saline and empty liposomes served as controls). Paw volume was measured with a plethysmometer. Hyperalgesia was determined by measuring heat-induced paw withdrawal latency and paw pressure threshold. Paw pressure threshold was also measured after swim stress and injection of fentanyl. RESULTS: At 48 and 96 h of inflammation, it was found that (1). monocytes/macrophages were the largest leukocyte subpopulation (> 55% of all leukocytes) and the predominant producers of opioid peptides (71-77% of all opioid-containing leukocytes in the paw), (2). clodronate-containing liposomes depleted monocytes/macrophages by 30-35% (P 0.05), and (4) opioid-containing leukocytes and swim stress but not fentanyl-induced antinociception were significantly decreased by clodronate-containing liposomes (P 0.05, all by t test; opioid-containing cells and swim stress-induced increase of paw pressure threshold were reduced by 35-42% and 20%, respectively). CONCLUSION: Partial depletion of tissue monocytes/macrophages impairs peripheral endogenous opioid-mediated antinociception without affecting hyperalgesia.
2004
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/00000542-200407000-00031" target="_blank" rel="noreferrer">10.1097/00000542-200407000-00031</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2004
Analgesics
Anesthesiology
Animals
Backlog
Biomarkers of Pain
Brack A
Clodronic Acid/pharmacokinetics/pharmacology
Fentanyl/administration & dosage/pharmacology
Flow Cytometry
Foot/pathology
Freund's Adjuvant
Heat
Hyperalgesia/chemically induced/pathology/psychology
Inflammation/chemically induced/pathology
Injections
Journal Article
Labuz D
Liposomes
Machelska H
Macrophages/pathology
Male
Monocytes/pathology
Non-Narcotic/pharmacokinetics/pharmacology
Opioid/administration & dosage/pharmacology
Pain Measurement/drug effects
Pressure
Rats
Reszka R
Rittner HL
Schafer M
Schiltz A
Stein C
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1213/00000539-200210000-00039" target="_blank" rel="noreferrer">http://doi.org/10.1213/00000539-200210000-00039</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Immune mechanisms in pain control
Publisher
An entity responsible for making the resource available
Anesthesia & Analgesia
Date
A point or period of time associated with an event in the lifecycle of the resource
2002
Subject
The topic of the resource
Humans; Analgesics; Animals; Non-U.S. Gov't; Research Support; Receptors; Immune System/physiology; Opioid/physiology; Opioid/pharmacology; Immunity; Endorphins/metabolism; Cellular/physiology; Pain/drug therapy/immunology/pathology
Creator
An entity primarily responsible for making the resource
Machelska H; Stein C
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1213/00000539-200210000-00039" target="_blank" rel="noreferrer">10.1213/00000539-200210000-00039</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
Description
An account of the resource
2002
2002
Analgesics
Anesthesia & Analgesia
Animals
Backlog
Cellular/physiology
Endorphins/metabolism
Humans
Immune System/physiology
Immunity
Journal Article
Machelska H
Non-U.S. Gov't
Opioid/pharmacology
Opioid/physiology
Pain/drug therapy/immunology/pathology
Receptors
Research Support
Stein C
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1046/j.1440-1681.2000.03287.x" target="_blank" rel="noreferrer">http://doi.org/10.1046/j.1440-1681.2000.03287.x</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Pain control by immune-derived opioids
Publisher
An entity responsible for making the resource available
Clinical And Experimental Pharmacology & Physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2000
Subject
The topic of the resource
Humans; Analgesics; Biomarkers of Pain; Receptors; Opioid/therapeutic use; Neuropeptides/therapeutic use; Opioid/drug effects/immunology; Pain/drug therapy/immunology; Peripheral Nervous System/drug effects
Creator
An entity primarily responsible for making the resource
Machelska H; Stein C
Description
An account of the resource
1. The nervous and immune systems communicate with each other by use of cytokines and neuropeptides. 2. Interactions between immune cell-derived opioid peptides and opioid receptors located in peripheral inflamed tissue lead to endogenous analgesia. 3. In addition to their immunological functions, immunocytes are involved in intrinsic pain inhibition. This provides new insights into pain associated with a compromised immune system, as in AIDS or in cancer. 4. The activation of opioid production and release from immune cells may be a novel approach to the development of peripherally acting analgesics. Because such drugs would be targeted towards events in peripheral injured tissue, these analgesics should lack unwanted central side effects typically associated with opioids.
2000
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1046/j.1440-1681.2000.03287.x" target="_blank" rel="noreferrer">10.1046/j.1440-1681.2000.03287.x</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2000
Analgesics
Backlog
Biomarkers of Pain
Clinical And Experimental Pharmacology & Physiology
Humans
Journal Article
Machelska H
Neuropeptides/therapeutic use
Opioid/drug effects/immunology
Opioid/therapeutic use
Pain/drug therapy/immunology
Peripheral Nervous System/drug effects
Receptors
Stein C
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1097/00000542-200108000-00036" target="_blank" rel="noreferrer">http://doi.org/10.1097/00000542-200108000-00036</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Opioid peptide-expressing leukocytes: identification, recruitment, and simultaneously increasing inhibition of inflammatory pain
Publisher
An entity responsible for making the resource available
Anesthesiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2001
Subject
The topic of the resource
Male; Pain Measurement; Analgesia; Animals; Rats; beta-Endorphin/blood; Biomarkers of Pain; Pain/physiopathology; Immunohistochemistry; Radioimmunoassay; Biomarkers Reference List; Wistar; Antibodies; Antigens; CD45/isolation & purification; Fluorescent Dyes; Hematopoietic Stem Cells/immunology; Immunomagnetic Separation; Inflammation/chemically induced/metabolism/pathology; Leukocytes/metabolism; Lymphocytes/immunology; Monoclonal/pharmacology; Opioid Peptides/biosynthesis
Creator
An entity primarily responsible for making the resource
Rittner HL; Brack A; Machelska H; Mousa SA; Bauer M; Schafer M; Stein C
Description
An account of the resource
BACKGROUND: Inflammatory pain can be effectively controlled by an interaction of opioid receptors on peripheral sensory nerve terminals with opioid peptides released from immune cells upon stressful stimulation. To define the source of opioid peptide production, we sought to identify and quantify populations of opioid-containing cells during the course of Freund's complete adjuvant-induced hind paw inflammation in the rat. In parallel, we examined the development of stress-induced local analgesia in the paw. METHODS: At 2, 6, and 96 h after Freund's complete adjuvant inoculation, cells were characterized by flow cytometry using a monoclonal pan-opioid antibody (3E7) and antibodies against cell surface antigens and by immunohistochemistry using a polyclonal antibody to beta-endorphin. After magnetic cell sorting, the beta-endorphin content was quantified by radioimmunoassay. Pain responses before and after cold water swim stress were evaluated by paw pressure thresholds. RESULTS: In early inflammation, 66% of opioid peptide-producing (3E7+) leukocytes were HIS48+ granulocytes. In contrast, at later stages (96 h), the majority of 3E7+ immune cells were ED1+ monocytes or macrophages (73%). During the 4 days after Freund's complete adjuvant inoculation, the number of 3E7+ cells increased 5.6-fold (P < 0.001, Kruskal-Wallis test) and the beta-endorphin content in the paw multiplied 3.9-fold (P < 0.05, Kruskal-Wallis test). In parallel, cold water swim stress-induced analgesia increased by 160% (P < 0.01, analysis of variance). CONCLUSIONS: The degree of endogenous pain inhibition is proportional to the number of opioid peptide-producing cells, and distinct leukocyte lineages contribute to this function at different stages of inflammation. These mechanisms may be important for understanding pain in immunosuppressed states such as cancer, diabetes, or AIDS and for the design of novel therapeutic strategies in inflammatory diseases.
2001
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/00000542-200108000-00036" target="_blank" rel="noreferrer">10.1097/00000542-200108000-00036</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2001
Analgesia
Anesthesiology
Animals
Antibodies
Antigens
Backlog
Bauer M
beta-Endorphin/blood
Biomarkers of Pain
Biomarkers Reference List
Brack A
CD45/isolation & purification
Fluorescent Dyes
Hematopoietic Stem Cells/immunology
Immunohistochemistry
Immunomagnetic Separation
Inflammation/chemically induced/metabolism/pathology
Journal Article
Leukocytes/metabolism
Lymphocytes/immunology
Machelska H
Male
Monoclonal/pharmacology
Mousa SA
Opioid Peptides/biosynthesis
Pain Measurement
Pain/physiopathology
Radioimmunoassay
Rats
Rittner HL
Schafer M
Stein C
Wistar