Ammonium pyrrolidine dithiocarbamate and RS 102895 attenuate opioid withdrawal in vivo and in vitro

Rehni, Ashish K.; Singh, Nirmal

doi:10.1007/s00213-011-2489-8

Cited by 8 publications

(4 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our data demonstrate that thymic MCP-1 expression is triggered in the thymus during Th1 inflammatory/infectious processes, thus facilitating the recruitment of certain peripheral CCR2 + T and B cells. To confirm this hypothesis, we treated T. cruzi infected mice with two specific antagonists of the MCP-1 ligand [29,30]. As can be seen in Fig.…”

Section: Expression Of Mcp-1 and Ccr2 Is Required For Extravasation Omentioning

confidence: 88%

“…To block CCR2 interaction with its ligand, RS 102895 (Sigma‐Aldrich, USA), a CCR2 antagonist was injected i.p. at 3 mg/kg in recipient mice twice, 24 h and 1 h before the adoptive transfer of cells and also CCR2 was blocked in CFSE‐labeled cells by incubation with the antagonist (10 μM) for 30 min before the adoptive transfer to recipient mice . To induce thymocyte apoptosis in vivo, dexamethasone (0.3 mg) was injected i.p.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

MCP‐1/CCR2 interactions direct migration of peripheral B and T lymphocytes to the thymus during acute infectious/inflammatory processes

et al. 2012

View full text Add to dashboard Cite

SUMMARY Mature lymphocyte immigration into the thymus has been documented in mouse, rat and pig models and highly increases when cells acquire an activated phenotype. Entrance of peripheral B and T cells into the thymus has been described in normal and pathological situations. However it has not been proposed that leukocyte recirculation to the thymus could be a common feature occurring during the early phase of a Th1 inflammatory/infectious process when a large number of peripheral cells acquire an activated phenotype and the cellularity of the thymus is seriously compromised. The data we present here demonstrate that in well-established Th1 models triggered by different types of immunogens, e.g. LPS treatment (a bacterial product), C. albicans infection (a fungus) and after T. cruzi infection (a parasite), a large number of mature peripheral B and T cells enter the thymus. This effect is dependent on, but not exclusive of, the available space in the thymus. Our data also demonstrate that MCP-1/CCR2 interaction is responsible for the infiltration of peripheral cells to the thymus in these Th1-inflammatory/infectious situations. Finally, systemic expression of IL-12 and IL-18 produced during the inflammatory process is ultimately responsible for these migratory events.

show abstract

Section: Expression Of Mcp-1 and Ccr2 Is Required For Extravasation Omentioning

confidence: 88%

Section: Methodsmentioning

confidence: 99%

MCP‐1/CCR2 interactions direct migration of peripheral B and T lymphocytes to the thymus during acute infectious/inflammatory processes

et al. 2012

View full text Add to dashboard Cite

show abstract

“…For therapeutic vaccination with HA, animals were vaccinated every 7 days until sacrifice due to progressive tumor growth. Animals were treated with the spiropiperidine small molecule compound, RS102895 (25–26)(Sigma-Aldrich) delivered by i.p. injection at a dose of 5 mg/kg twice daily, starting the day before, the day of, and the day following vaccination and boost.…”

Section: Methodsmentioning

confidence: 99%

Suppression of Vaccine Immunity by Inflammatory Monocytes

Mitchell

Henderson

Dow

2012

The Journal of Immunology

View full text Add to dashboard Cite

Vaccine adjuvant-induced inflammation augments vaccine immunity in part by recruiting antigen presenting cells to vaccine draining lymph nodes. However, the role of one antigen presenting cell subtype, inflammatory monocytes, in regulating vaccine immunity in healthy animals has not been fully examined in detail. Therefore, vaccine-mediated monocyte recruitment and subsequent immune responses were investigated using murine vaccination models and in vitro assays. Recruitment of inflammatory monocytes to vaccine draining lymph nodes was rapid and mediated primarily by local production of MCP-1, as revealed by studies in MCP-1−/− mice. Interrupting monocyte recruitment to lymph nodes by either transient monocyte depletion or monocyte migration blockade led to marked amplification of both cellular and humoral immune responses to vaccination. These results were most consistent with the idea that rapidly mobilized inflammatory monocytes were actually suppressing vaccine responses. The suppressive nature of vaccine-elicited monocytes was confirmed using in vitro co-cultures of murine monocytes and T cells. Furthermore, it was determined that inflammatory monocytes suppressed T cell responses by sequestering cysteine, as cysteine supplementation in vitro and in vivo appreciably augmented vaccine responses. These findings indicated therefore that vaccination-elicited inflammation, while necessary for effective immunity, also generated potent counter-regulatory immune responses that were mediated primarily by inflammatory monocytes. Therefore, interrupting monocyte mediated vaccine counter-regulatory responses may serve as an effective new strategy for broadly amplifying vaccine immunity.

show abstract

“…A dose of either 3.0 mg/kg RS 102895 or DMSO (vehicle) was given to separate cohorts of six mice to inhibit the function of CCR2. The dose was selected based on its efficacy in previously published studies [53, 54]. …”

Section: Resultsmentioning

confidence: 99%

The effect of inflammatory cell-derived MCP-1 loss on neuronal survival during chronic neuroinflammation

et al. 2014

View full text Add to dashboard Cite

Intracranial implants elicit neurodegeneration via the foreign body response (FBR) that includes BBB leakage, macrophage/microglia accumulation, and reactive astrogliosis, in addition to neuronal degradation that limit their useful lifespan. Previously, monocyte chemoattractant protein 1 (MCP-1, also CCL2), which plays an important role in monocyte recruitment and propagation of inflammation, was shown to be critical for various aspects of the FBR in a tissue-specific manner. However, participation of MCP-1 in the brain FBR has not been evaluated. Here we examined the FBR to intracortical silicon implants in MCP-1 KO mice at 1, 2, and 8 weeks after implantation. MCP-1 KO mice had a diminished FBR compared to WT mice, characterized by reductions in BBB leakage, macrophage/microglia accumulation, and astrogliosis, and an increased neuronal density. Moreover, pharmacological inhibition of MCP-1 in implant-bearing WT mice maintained the increased neuronal density. To elucidate the relative contribution of microglia and macrophages, bone marrow chimeras were generated between MCP-1 KO and WT mice. Increased neuronal density was observed only in MCP-1 knockout mice transplanted with MCP-1 knockout marrow, which indicates that resident cells in the brain are major contributors. We hypothesized that these improvements are the result of a phenotypic switch of the macrophages/microglia polarization state, which we confirmed using PCR for common activation markers. Our observations suggest that MCP-1 influences neuronal loss, which is integral to the progression of neurological disorders like Alzheimer’s and Parkinson disease, via BBB leakage and macrophage polarization.

show abstract

Ammonium pyrrolidine dithiocarbamate and RS 102895 attenuate opioid withdrawal in vivo and in vitro

Abstract: It is concluded that APD and RS 102895 attenuate morphine withdrawal signs possibly by a NF-κB and C-C chemokine receptor 2 activation pathway-linked mechanisms potentially in an interdependent manner.

Cited by 8 publications

References 43 publications

MCP‐1/CCR2 interactions direct migration of peripheral B and T lymphocytes to the thymus during acute infectious/inflammatory processes

MCP‐1/CCR2 interactions direct migration of peripheral B and T lymphocytes to the thymus during acute infectious/inflammatory processes

Suppression of Vaccine Immunity by Inflammatory Monocytes

The effect of inflammatory cell-derived MCP-1 loss on neuronal survival during chronic neuroinflammation

Contact Info

Product

Resources

About