Effect of Prostaglandin I<sub>2</sub> Analogs on Macrophage Inflammatory Protein 1α in Human Monocytes via I Prostanoid Receptor and Cyclic Adenosine Monophosphate

Tsai, Ming-Kai; Hsieh, Chong‐Chao; Kuo, Hsuan-Fu; Yang, San‐Nan; Kuo, Chang-Hung; Tsai, Yi-Hsuan; Lee, Min‐Sheng; Hung, Chih‐Hsing

doi:10.2310/jim.0000000000000042

Cited by 7 publications

(7 citation statements)

References 21 publications

(34 reference statements)

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“…PGs E 2 and I 2 , and cysteinyl leukotrienes). In turn, these eicosanoids can modulate chemokine production in monocytes and macrophages (Hashimoto et al ., ; Ichiyama et al ., ; Kuo et al ., ; Buenestado et al ., ; Tsai et al ., ). Furthermore, 15‐HETE can be also produced via COX‐dependent pathways (Levy et al ., ).…”

Section: Discussionmentioning

confidence: 97%

15‐Lipoxygenases regulate the production of chemokines in human lung macrophages

Abrial

Grassin-Delyle

Salvator

et al. 2015

British J Pharmacology

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BACKGROUND AND PURPOSE15-Lipoxygenase (15-LOX) activity is associated with inflammation and immune regulation. The objectives of the present study were to investigate the expression of 15-LOX-1 and 15-LOX-2 and evaluate the enzymes' roles in the polarization of human lung macrophages (LMs) in response to LPS and Th2 cytokines (IL-4/-13). EXPERIMENTAL APPROACHLMs were isolated from patients undergoing surgery for carcinoma. The cells were cultured with a 15-LOX inhibitor (PD146176 or ML351), a COX inhibitor (indomethacin), a 5-LOX inhibitor (MK886) or vehicle and then stimulated with LPS (10 ng·mL ) for 24 h. Levels of ALOX15 (15-LOX-1) and ALOX15B (15-LOX-2) transcripts were determined by real-time quantitative PCR. Immunoassays were used to measure levels of LPS-induced cytokines (TNF-α, CCL2, CCL3, CCL4, CXCL1, CXCL8 and CXCL10) and Th2 cytokine-induced chemokines (CCL13, CCL18 and CCL22) in the culture supernatant. KEY RESULTSStimulation of LMs with LPS was associated with increased expression of ALOX15B, whereas stimulation with IL-4/IL-13 induced the expression of ALOX15. PD146176 and ML351 (10 μM) reduced the release of the chemokines induced by LPS and Th2 cytokines. The effects of these 15-LOX inhibitors were maintained in the presence of indomethacin and MK886. Furthermore, indomethacin revealed the inhibitory effect of PD146176 on TNF-α release. CONCLUSIONS AND IMPLICATIONSInhibition of the 15-LOX pathways is involved in the down-regulation of the in vitro production of chemokines in LMs. Our results suggest that the 15-LOX pathways have a role in the pathogenesis of inflammatory lung disorders and may thus constitute a potential drug target. AbbreviationsFCS, fetal calf serum; 15-HETE, 15-hydroxyeicosatetraenoic acid; 13-HODE, 13-hydroxy octadecadienoic acid; HPRT, hypoxanthine phosphoribosyltransferase; LM, lung macrophage; LOX, lipoxygenase; MDM, monocyte-derived macrophage BJP British Journal of Pharmacology

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Section: Discussionmentioning

confidence: 97%

15‐Lipoxygenases regulate the production of chemokines in human lung macrophages

Abrial

Grassin-Delyle

Salvator

et al. 2015

British J Pharmacology

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“…Moreover, PGI 2 has inhibitory effects on the activation of endothelial cells and on the proliferation and migration of smooth muscle cells (41)(42)(43). PGI 2 acts on leukocytes stimulating the production of anti-inflammatory cytokines and inhibiting the release of IL-1, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ. PGI 2 also regulates macrophage functions, promoting their anti-inflammatory profile (44,45). Effects on the inhibition of platelet aggregation have also been described (20,43).…”

Section: Discussionmentioning

confidence: 99%

Iloprost in Acute Post-kidney Transplant Atheroembolism: A Case Report of Two Successful Treatments

et al. 2020

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Cholesterol embolization (CE) is a rare and alarming post-transplant complication, responsible for primary non-function (PNF) or delayed graft function (DGF). Its incidence is expected to rise due to increasingly old donors and recipients and the extended criteria for donation. Therapy with statins and steroids has not been shown to be effective, while agonism of prostaglandin I 2 has been reported to be useful in systemic CE. We report two cases of acute post-transplant CE in which intravenous iloprost (0.05 mg/kg/day) was added to standard statin and steroid therapy. In the first instance, CE was due to embolization from the kidney artery resulting in embolization of the small vessels; after a long DGF and 15 days of iloprost therapy, renal function recovered. The second instance is a case of embolization from the iliac artery of the recipient, where CE manifested as a partial renal infarction. After 5 days of iloprost administration, creatinine levels improved. Iloprost acts on vasodilation and on different inflammatory pathways, improving the anti-inflammatory profile. Post-transplant CE is difficult to diagnose and, if not treated, can lead to loss of function. Iloprost added to standard therapy could be beneficial in accelerating renal function recovery immediately after transplant.

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“…Additionally, PPARα can regulate the expression of other chemokines, such as macrophage inflammatory protein-1α (MIP-1α). Tsai et al have reported that prostaglandin I2 analogs inhibit LPS-induced MIP-1α production in THP-1 cells and human primary monocytes by upregulation of PPARα [100]. Overall, PPARα-mediated downregulation of MCP-1 and MIP-1α also plays critical roles in the limitation of vascular inflammation during atherogenesis.…”

Section: Pparα Limits Vascular Inflammationmentioning

confidence: 91%

Peroxisome Proliferator-Activated Receptor α in Lipid Metabolism and Atherosclerosis

Zheng

Tang

2015

Advances in Clinical Chemistry

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Effect of Prostaglandin I₂ Analogs on Macrophage Inflammatory Protein 1α in Human Monocytes via I Prostanoid Receptor and Cyclic Adenosine Monophosphate

Abstract: Prostaglandin I2 analogs suppressed LPS-induced MIP-1α production in human monocytes via the IP receptor and cAMP pathway. The PGI2 analog may be potential in the treatment for atherosclerosis.

Cited by 7 publications

References 21 publications

15‐Lipoxygenases regulate the production of chemokines in human lung macrophages

15‐Lipoxygenases regulate the production of chemokines in human lung macrophages

Iloprost in Acute Post-kidney Transplant Atheroembolism: A Case Report of Two Successful Treatments

Peroxisome Proliferator-Activated Receptor α in Lipid Metabolism and Atherosclerosis

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Effect of Prostaglandin I2 Analogs on Macrophage Inflammatory Protein 1α in Human Monocytes via I Prostanoid Receptor and Cyclic Adenosine Monophosphate

Abstract: Prostaglandin I2 analogs suppressed LPS-induced MIP-1α production in human monocytes via the IP receptor and cAMP pathway. The PGI2 analog may be potential in the treatment for atherosclerosis.

Cited by 7 publications

References 21 publications

15‐Lipoxygenases regulate the production of chemokines in human lung macrophages

15‐Lipoxygenases regulate the production of chemokines in human lung macrophages

Iloprost in Acute Post-kidney Transplant Atheroembolism: A Case Report of Two Successful Treatments

Peroxisome Proliferator-Activated Receptor α in Lipid Metabolism and Atherosclerosis

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Product

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Effect of Prostaglandin I₂ Analogs on Macrophage Inflammatory Protein 1α in Human Monocytes via I Prostanoid Receptor and Cyclic Adenosine Monophosphate