Modulation of chemiluminescence in a murine macrophage cell line by neuroendocrine hormones

Tosk, Jeffrey M.; Grim, Joseph R.; Kinback, Kevin M.; Sale, E. Jeffrey; Bozzetti, Louis P.; Will, Albrecht

doi:10.1016/0192-0561(93)90079-e

Cited by 33 publications

(14 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Similarly, the x-agonist U50488 was reported to inhibit significantly mouse splenocyte activity [28] while no x transcript was found in our analysis of murine spleen RNA. Another discrepancy is our finding that none of the cloned opioid receptor is expressed in J774 cells, which have been shown to effectively respond to Dynorphin A in a naloxone-reversible manner [33]. This apparent lack of correspondence might arise from high interindividual variability in humans, as was previously shown for naloxone binding on T lymphocytes [34] or opioid effects on PBL Table 1 Summary of opioid receptor expression in human and mouse immune cells proliferation [35], or be related to strain-dependent immune response in mice [36], or finally be due to the existence of divergent subclones in the model cell lines that we have used.…”

Section: Discussioncontrasting

confidence: 46%

Identification of κ‐ and δ‐opioid receptor transcripts in immune cells

et al. 1995

View full text Add to dashboard Cite

To investigate the role of opioids as direct modulators of the immune response, we have searched for expression of the recently cloned 6,/~ and K opioid receptors in immune cells. We have devised a reverse transcriptase-polymerase chain reaction strategy which specifically detects a region spanning putative transmembrane regions 2 to 7 for each transcript in both human and mouse immune cells. In human peripheral blood lymphocyte and monocyte preparations, 6 was undetectable while the g transcript was present. The analysis of human cell lines revealed low but significant levels of 6 opioid receptor transcripts in T, B or monocyte cell lines while the K transcript was found in B cell lines only. Investigation of routine cells showed the presence of transcript for the 6 receptor in splenocytes and in some T and B cell lines. Unexpectedly, no expression of the bt receptor was detected. Sequence analysis of PCR products demonstrated nucleotide identity between immune and neuronal transcripts, indicating that they derive from the same genes. In conclusion, our results lead to the identification of K and 6 opioid receptor transcripts in immune cells.

show abstract

Section: Discussioncontrasting

confidence: 46%

Identification of κ‐ and δ‐opioid receptor transcripts in immune cells

et al. 1995

View full text Add to dashboard Cite

show abstract

“…These results suggest that endogenous activation of κ opioid receptors may exert a tonic inhibition of antibody responses. The endogenous κ-selective peptide, dynorphin, has been shown to increase macrophage superoxide production (Sharp et al 1985), modulate macrophage oxidative burst (Tosk et al 1993), enhance macrophage tumoricidal activity (Foster and Moore 1987;Hagi et al 1994) and increase production of the cytokine IL-1 from bone marrow macrophages (Apte et al 1990). In the macrophage cell line P388D 1 , the κ-selective agonist, U50,488, inhibited the synthesis of IL-1 and TNF-α (Belkowski et al 1995a).…”

Section: Functional Evidence For the Presence Of Kappa Opioid Receptomentioning

confidence: 98%

Opioid Receptors and Signaling on Cells from the Immune System

Bidlack

Khimich

Parkhill

et al. 2006

Jrnl Neuroimmune Pharm

View full text Add to dashboard Cite

This review discusses the criteria for determining whether a binding site or functional response is directly mediated by either the mu, delta, or kappa opioid receptors. In 1988, Sibinga and Goldstein published the first review that addressed whether cells from the immune system express opioid receptors. The criteria that they used, namely, structure-activity relationships, stereoselectivity, dose- and concentration-dependence, and saturability are still relevant criteria today for determining if an immunological response is mediated by either the mu, delta or kappa opioid receptors. Radioligand receptor binding studies and functional studies that clearly show the presence of an opioid receptor on immunocytes are presented. Selective agonists and antagonists for the mu, delta, and kappa opioid receptors are discussed, and the need for their use in experiments is emphasized. Conditions used in functional assays are very important. Receptor desensitization and downregulation occur within minutes after the application of an agonist. However, many immunological assays are applying an agonist for days before measuring an immunological effect. The results obtained may reflect changes that are results of receptor desensitization and/or downregulation instead of changes that are observed with acute activation of the receptor. The future of receptor pharmacology lies in the crosstalk and dimerization of G protein-coupled receptors. In transfected systems, opioid receptors have been shown to dimerize with chemokine and cannabinoid receptors, resulting in crosstalk between different types of receptors.

show abstract

“…The endogenous kappa selective peptide, dynorphin, has been shown to increase macrophage superoxide production [40], modulate macrophage oxidative burst [41], enhance macrophage tumoricidal activity [42,43] and increase production of the cytokine IL-1 from bone marrow macrophages [44]. Both T cells and macrophages are targets for kappa agonists to produce inhibition of T-cell-mediated antibody production [12,45,46].…”

Section: Discussionmentioning

confidence: 99%

Trigeminal Injury Causes kappa Opioid-Dependent Allodynic, Glial and Immune Cell Responses in Mice

et al. 2010

View full text Add to dashboard Cite

BackgroundThe dynorphin-kappa opioid receptor (KOR) system regulates glial proliferation after sciatic nerve injury. Here, we investigated its role in cell proliferation following partial ligation of infraorbital nerve (pIONL), a model for trigeminal neuropathic pain. Mechanical allodynia was enhanced in KOR gene deleted mice (KOR-/-) compared to wild type mice. Using bromodeoxyuridine (BrdU) as a mitotic marker, we assessed cell proliferation in three different areas of the trigeminal afferent pathway: trigeminal nucleus principalis (Vp), trigeminal root entry zone (TREZ), and trigeminal ganglion (TG).ResultsIn KOR-/- mice or norBNI-treated mice, the number of proliferating cells in the Vp was significantly less than in WT mice, whereas cell proliferation was enhanced in TREZ and TG. The majority of the proliferating cells were nestin positive stem cells or CD11b positive microglia in the Vp and macrophages in the TG. GFAP-positive astrocytes made a clear borderline between the CNS and the PNS in TREZ, and phosphorylated KOR staining (KOR-p) was detectable only in the astrocytes in CNS in WT mice but not in KOR-/- or norBNI-treated mice.ConclusionsThese results show that kappa opioid receptor system has different effects after pIONL in CNS and PNS: KOR activation promotes CNS astrocytosis and microglial or stem cell proliferation but inhibits macrophage proliferation in PNS. The trigeminal central root has a key role in the etiology and treatment of trigeminal neuralgia, and these newly identified responses may provide new targets for developing pain therapies.

show abstract

Modulation of chemiluminescence in a murine macrophage cell line by neuroendocrine hormones

Cited by 33 publications

References 26 publications

Identification of κ‐ and δ‐opioid receptor transcripts in immune cells

Identification of κ‐ and δ‐opioid receptor transcripts in immune cells

Opioid Receptors and Signaling on Cells from the Immune System

Trigeminal Injury Causes kappa Opioid-Dependent Allodynic, Glial and Immune Cell Responses in Mice

Contact Info

Product

Resources

About