Control of inflammatory pain by chemokine-mediated recruitment of opioid-containing polymorphonuclear cells

Title

Control of inflammatory pain by chemokine-mediated recruitment of opioid-containing polymorphonuclear cells

Creator

Brack A; Rittner HL; Machelska H; Leder K; Mousa SA; Schafer M; Stein C

Publisher

Pain

Date

2004

Subject

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

Description

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

Rights

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

Journal Article

Citation List Month

Backlog

Pages

229-238

Issue

3

Volume

112

Citation

Brack A; Rittner HL; Machelska H; Leder K; Mousa SA; Schafer M; Stein C, “Control of inflammatory pain by chemokine-mediated recruitment of opioid-containing polymorphonuclear cells,” Pediatric Palliative Care Library, accessed October 28, 2021, https://pedpalascnetlibrary.omeka.net/items/show/13042.

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