Effect of dexamethasone and meloxicam on counts of selected T lymphocyte subpopulations and NK cells in cattle – In vivo investigations

Maślanka, Tomasz

doi:10.1016/j.rvsc.2014.02.006

Cited by 12 publications

(6 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Selective COX-2 inhibitors, including meloxicam, are launched and widely used as anti-inflammatory compounds in the dairy and beef industries. Previous studies have investigated the in vivo effect of meloxicam on T-cell subsets in healthy or vaccinated cattle (43,44). However, the in vivo effect of meloxicam on the Th1 response during Johne's disease is still unclear and should be determined in further experiments in infected cattle.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E₂Induction Suppresses the Th1 Immune Responses in Cattle with Johne's Disease

et al. 2018

View full text Add to dashboard Cite

Johne's disease, caused by subsp., is a bovine chronic infection that is endemic in Japan and many other countries. The expression of immunoinhibitory molecules is upregulated in cattle with Johne's disease, but the mechanism of immunosuppression is poorly understood. Prostaglandin E (PGE) is immunosuppressive in humans, but few veterinary data are available. In this study, functional and kinetic analyses of PGE were performed to investigate the immunosuppressive effect of PGE during Johne's disease. PGE treatment decreased T-cell proliferation and Th1 cytokine production and upregulated the expression of immunoinhibitory molecules such as interleukin-10 and programmed death ligand 1 (PD-L1) in peripheral blood mononuclear cells (PBMCs) from healthy cattle. PGE was upregulated in sera and intestinal lesions of cattle with Johne's disease. stimulation with Johnin purified protein derivative (J-PPD) induced cyclooxygenase-2 (COX-2) transcription, PGE production, and upregulation of PD-L1 and immunoinhibitory receptors in PBMCs from cattle infected with subsp. Therefore, Johnin-specific Th1 responses could be limited by the PGE pathway in cattle. In contrast, downregulation of PGE with a COX-2 inhibitor promoted J-PPD-stimulated CD8 T-cell proliferation and Th1 cytokine production in PBMCs from the experimentally infected cattle. PD-L1 blockade induced J-PPD-stimulated CD8 T-cell proliferation and interferon gamma production Combined treatment with a COX-2 inhibitor and anti-PD-L1 antibodies enhanced J-PPD-stimulated CD8 T-cell proliferation , suggesting that the blockade of both pathways is a potential therapeutic strategy to control Johne's disease. The effects of COX-2 inhibition warrant further study as a novel treatment of Johne's disease.

show abstract

Section: Discussionmentioning

confidence: 99%

Prostaglandin E₂Induction Suppresses the Th1 Immune Responses in Cattle with Johne's Disease

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Our results are in agreement with the data obtained by Iñiguez et al [13], who also demonstrated that a preferential COX-1 inhibitor (indomethacin) had no effect on the activation-induced CD25 expression on CD3 + cells, whereas a selective COX-2 inhibitor (NS398) down-regulated it. Furthermore, our previous studies showed that meloxicam, a preferential COX-2 inhibitor, reduced constitutive CD25 expression on bovine CD4 + , CD8 + and WC1 + T cells [8-11]. Besides, it was demonstrated that non-preferential COX inhibitors (ibuprofen and naproxen) significantly inhibited the proliferative response of T cells to IL-2, while preferential COX-1 inhibitors (indomethacin and piroxicam) did not alter this response.…”

Section: Discussionmentioning

confidence: 99%

“…Perusal of the available literature has shown a shortage of research on the effect of NSAIDs on CD25 expression on CD4 + and CD8 + T cells during their activation. In our previous investigations [8-11], we evaluated the influence of meloxicam (a NSAID) on the expression of CD25 by bovine peripheral blood T cells, but our research only dealt with constitutive, and not with activation-induced, expression. These studies demonstrated that the drug significantly down-regulated CD25 expression on CD4 + , CD8 + and WC1 + T cells, although the effect did not manifest itself very strongly.…”

Section: Introductionmentioning

confidence: 99%

Effect of selected non-steroidal anti-inflammatory drugs on activation-induced CD25 expression on murine CD4+ and CD8+ T cells: an in vitro study

Gregorczyk

Maślanka

2019

cejoi

Self Cite

View full text Add to dashboard Cite

The main aim of this study has been to determine the effect of selected non-steroidal anti-inflammatory drugs (NSAIDs) – depending on their selectivity to cyclooxygenase (COX) 1 and 2 – on the activation-induced CD25 expression on CD4+ and CD8+ T cells. Lymphocytes obtained from lymph nodes of mice were treated with acetylsalicylic acid (ASA; a preferential COX-1 inhibitor), ketoprofen (KET; a non-selective COX inhibitor) and robenacoxib (ROB; a selective COX-2 inhibitor) in concentrations reflecting their plasma levels achieved in vivo at therapeutic doses and in ten-fold lower concentrations. The cells were activated with concanavalin A. In contrast to KET and ROB, ASA had no effect on the activation-induced CD25 expression on CD4+ and CD8+ T cells, nor did it affect the counts of CD4+ and CD8+ activated effector (aTeff) and resting (Trest) T cells. Both KET and ROB caused a depletion of CD8+ aTeff cells, and additionally KET induced a loss of CD8+ Trest cells. Moreover, ROB, but not the other drugs, reduced the activation-induced CD25 expression on CD4+ T cells. This suggests that non-selective COX inhibitors and selective COX-2 inhibitors may weaken the effector T cell response by producing a negative effect on the count of aTeff cells. Furthermore, the results seem to imply that ASA and KET have certain potential to induce Foxp3 expression in CD25+CD8+ and CD25+CD4+ T cells, respectively. However, all the observed changes were very weakly manifested and therefore it is not certain whether they have clinical importance, despite the statistical significance determined.

show abstract

“…MEL (M3935, Sigma-Aldrich, USA) was dissolved in DMSO and stored at −20 • C. It has been reported that the injection dose of 0.5 mg/kg MEL could maintain the blood concentration of 0.2 µg/ml MEL in cows with endometritis (22). In addition, MEL was used in a bovine lymphocyte test (23,24), which provided references for MEL concentration in this experiment.…”

Section: Mel Treatmentmentioning

confidence: 99%

Meloxicam Inhibited the Proliferation of LPS-Stimulated Bovine Endometrial Epithelial Cells Through Wnt/β-Catenin and PI3K/AKT Pathways

Cui

Cai

et al. 2021

Front. Vet. Sci.

View full text Add to dashboard Cite

Meloxicam is a non-steroidal anti-inflammatory drug and has been used to relieve pain and control inflammation in cows with metritis and endometritis. Meloxicam has been found to be effective in inhibiting tissue or cell growth when it is used as an anti-inflammatory therapy. However, the influence of meloxicam on bovine endometrial regeneration has not been reported. This study was to research the effect of meloxicam (0.5 and 5 μM) on the proliferation of primary bovine endometrial epithelial cells (BEECs) stimulated by Escherichia coli lipopolysaccharide. The cell viability, cell cycle, and cell proliferation were evaluated by Cell Counting Kit-8, flow cytometry, and cell scratch test, respectively. The mRNA transcriptions of prostaglandin-endoperoxide synthase 1 (PTGS1) and PTGS2, Toll-like receptor 4, and proliferation factors were detected using quantitative reverse-transcription polymerase chain reaction. The activations of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) and Wnt/β-catenin pathways were determined using western blot and immunofluorescence. As a result, co-treatment of meloxicam and lipopolysaccharide inhibited (P < 0.05) the cell cycle progression and reduced (P < 0.05) the cell healing rate and the mRNA level of proliferation factors as compared with the cells treated with lipopolysaccharide alone. Meloxicam decreased (P < 0.05) the lipopolysaccharide-induced PTGS2 gene expression. Neither lipopolysaccharide nor meloxicam changed PTGS1 mRNA abundance (P > 0.05). Meloxicam inhibited (P < 0.05) the lipopolysaccharide-activated Wnt/β-catenin pathway by reducing (P < 0.05) the protein levels of β-catenin, c-Myc, cyclin D1, and glycogen synthase kinase-3β and prevented the lipopolysaccharide-induced β-catenin from entering the nucleus. Meloxicam suppressed (P < 0.05) the phosphorylation of PI3K and AKT. In conclusion, meloxicam alone did not influence the cell cycle progression or the cell proliferation in BEEC but caused cell cycle arrest and inhibited cell proliferation in lipopolysaccharide-stimulated BEEC. This inhibitory effect of meloxicam was probably mediated by Wnt/β-catenin and PI3K/AKT pathways.

show abstract

Effect of dexamethasone and meloxicam on counts of selected T lymphocyte subpopulations and NK cells in cattle – In vivo investigations

Cited by 12 publications

References 20 publications

Prostaglandin E₂Induction Suppresses the Th1 Immune Responses in Cattle with Johne's Disease

Prostaglandin E₂Induction Suppresses the Th1 Immune Responses in Cattle with Johne's Disease

Effect of selected non-steroidal anti-inflammatory drugs on activation-induced CD25 expression on murine CD4+ and CD8+ T cells: an in vitro study

Meloxicam Inhibited the Proliferation of LPS-Stimulated Bovine Endometrial Epithelial Cells Through Wnt/β-Catenin and PI3K/AKT Pathways

Contact Info

Product

Resources

About

Effect of dexamethasone and meloxicam on counts of selected T lymphocyte subpopulations and NK cells in cattle – In vivo investigations

Cited by 12 publications

References 20 publications

Prostaglandin E2Induction Suppresses the Th1 Immune Responses in Cattle with Johne's Disease

Prostaglandin E2Induction Suppresses the Th1 Immune Responses in Cattle with Johne's Disease

Effect of selected non-steroidal anti-inflammatory drugs on activation-induced CD25 expression on murine CD4+ and CD8+ T cells: an in vitro study

Meloxicam Inhibited the Proliferation of LPS-Stimulated Bovine Endometrial Epithelial Cells Through Wnt/β-Catenin and PI3K/AKT Pathways

Contact Info

Product

Resources

About

Prostaglandin E₂Induction Suppresses the Th1 Immune Responses in Cattle with Johne's Disease

Prostaglandin E₂Induction Suppresses the Th1 Immune Responses in Cattle with Johne's Disease