Immunomodulatory Actions of Lysophosphatidylcholine

Hong, Chang-Won; Song, Dong‐Keun

doi:10.4062/biomolther.2008.16.2.069

Cited by 7 publications

(6 citation statements)

References 65 publications

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“…Lysophosphatidylcholine can recruit immune cells and modulate their function, especially in neutrophils and T cells, and it may play a role in the control of bacterial growth during infection ( 28 ). To verify whether LPC possesses mycobactericidal activity, mouse macrophages were infected with avirulent or virulent Mtb, H37Ra or H37Rv, respectively, at an MOI of 0.1 or 1 and then treated them with LPC (Figure 1 ).…”

Section: Resultsmentioning

confidence: 99%

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Lysophosphatidylcholine Promotes Phagosome Maturation and Regulates Inflammatory Mediator Production Through the Protein Kinase A–Phosphatidylinositol 3 Kinase–p38 Mitogen-Activated Protein Kinase Signaling Pathway During Mycobacterium tuberculosis Infection in Mouse Macrophages

Lee

Song

et al. 2018

Front. Immunol.

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Tuberculosis is caused by the infectious agent Mycobacterium tuberculosis (Mtb). Mtb has various survival strategies, including blockade of phagosome maturation and inhibition of antigen presentation. Lysophosphatidylcholine (LPC) is a major phospholipid component of oxidized low-density lipoprotein and is involved in various cellular responses, such as activation of second messengers and bactericidal activity in neutrophils. In this study, macrophages were infected with a low infectious dose of Mtb and treated with LPC to investigate the bactericidal activity of LPC against Mtb. In macrophages infected with Mtb strain, H37Ra or H37Rv, LPC suppressed bacterial growth; however, this effect was suppressed in bone marrow-derived macrophages (BMDMs) isolated from G2A (a G protein-coupled receptor involved in some LPC actions) knockout mice. LPC also promoted phagosome maturation via phosphatidylinositol 3 kinase (PI3K)–p38 mitogen-activated protein kinase (MAPK)-mediated reactive oxygen species production and intracellular Ca2+ release during Mtb infection. In addition, LPC induced increased levels of intracellular cyclic adenosine monophosphate (cAMP) and phosphorylated glycogen synthase kinase 3 beta (GSK3β) in Mtb-infected macrophages. Protein kinase A (PKA)-induced phosphorylation of GSK3β suppressed activation of NF-κB in LPC-treated macrophages during Mtb infection, leading to decreased secretion of pro-inflammatory cytokines and increased secretion of anti-inflammatory cytokines. These results suggest that LPC can effectively control Mtb growth by promoting phagosome maturation via cAMP-induced activation of the PKA–PI3K–p38 MAPK pathway. Moreover, LPC can regulate excessive production of pro-inflammatory cytokines associated with bacterial infection of macrophages.

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Section: Resultsmentioning

confidence: 99%

“…Lysophosphatidylcholine, an endogenous phospholipid, has various stimulating or modulating effects on immune cells, such as monocytes/macrophages, neutrophils, and lymphocytes ( 28 ). Most studies have demonstrated pro-inflammatory activities of LPC; however, LPC possesses anti-inflammatory properties.…”

Section: Discussionmentioning

confidence: 99%

Lysophosphatidylcholine Promotes Phagosome Maturation and Regulates Inflammatory Mediator Production Through the Protein Kinase A–Phosphatidylinositol 3 Kinase–p38 Mitogen-Activated Protein Kinase Signaling Pathway During Mycobacterium tuberculosis Infection in Mouse Macrophages

Lee

Song

et al. 2018

Front. Immunol.

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“…Monocytes/macrophages are the prime immune cells managing inflammatory responses, which contribute to development of number of diseases such as cancer, diabetes, and atherosclerosis [ 30 , 31 ]. This view led us to develop novel immunoregulatory drugs based on the functional activation of monocytes and macrophages without side effects to prevent such diseases.…”

Section: Resultsmentioning

confidence: 99%

Regulatory Effect of Cinnamaldehyde on Monocyte/Macrophage-Mediated Inflammatory Responses

Kim

Lee

et al. 2010

Mediators of Inflammation

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Cinnamaldehyde (CA) has been known to exhibit anti-inflammatory and anticancer effects. Although numerous pharmacological effects have been demonstrated, regulatory effect of CA on the functional activation of monocytes and macrophages has not been fully elucidated yet. To evaluate its monocyte/macrophage-mediated immune responses, macrophages activated by lipopolysaccharide (LPS), and monocytes treated with proaggregative antibodies, and extracellular matrix protein fibronectin were employed. CA was able to suppress both the production of nitric oxide (NO) and upregulation of surface levels of costimulatory molecules (CD80 and CD69) and pattern recognition receptors (toll-like receptor 2 (TLR2) and complement receptor (CR3)). In addition, CA also blocked cell-cell adhesion induced by the activation of CD29 and CD43 but not cell-fibronectin adhesion. Immunoblotting analysis suggested that CA inhibition was due to the inhibition of phosphoinositide-3-kinase (PI3K) and phosphoinositide-dependent kinase (PDK)1 as well as nuclear factor-(NF-) κB activation. In particular, thiol compounds with sulphydryl group, L-cysteine and dithiothreitol (DTT), strongly abrogated CA-mediated NO production and NF-κB activation. Therefore, our results suggest that CA can act as a strong regulator of monocyte/macrophage-mediated immune responses by thiolation of target cysteine residues in PI3K or PDK1.

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“…Under inflammatory conditions, LPCs can be generated by reactive oxygen species (ROS) . Some type of LPCs can release highly unsaturated arachidonic acid that is readily converted into compounds with either pro‐ or anti‐inflammatory effects . Downregulation of LPCs may reflect disturbed inflammation in ONFH.…”

Section: Discussionmentioning

confidence: 99%

Unique plasma metabolomic signature of osteonecrosis of the femoral head

Liu

Sheng

et al. 2015

Journal Orthopaedic Research

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Metabolomic analysis was performed to determine the metabolomic signature of osteonecrosis of the femoral head (ONFH), and to investigate the underlying relationship between the metabolomic signature and the pathogenesis of ONFH. Plasma samples were collected from 30 ONFH patients and 30 normal subjects. The global metabolomic profile was obtained through a combination of high-throughput liquid-and gas-chromatography-based mass spectrometry analyses. All statistical analyses were conducted using the R software. The results showed clear differences in the metabolomic signature between the plasma of ONFH patients compared with normal subjects. Among the 354 identified metabolites, the expression of 123 metabolites were significantly changed in ONFH patients compared with normal subjects (p < 0.05, q < 0.10). Bioinformatics analysis revealed that these abnormal metabolites were mainly involved in lipid-, glutathione-, nucleotide-, and energy-associated pathways, which might be related to enhanced inflammation, oxidative stress, and energy deficiency due to ONFH. This study provides the first metabolomic analysis of ONFH, and identifies a previously unrecognized metabolic signature in ONFH plasma. The results offer new insights into the pathological mechanisms of ONFH through its influence on metabolic pathways, providing the requisite framework for identifying biomarkers or novel targets for therapeutic intervention. ß

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Immunomodulatory Actions of Lysophosphatidylcholine

Cited by 7 publications

References 65 publications

Lysophosphatidylcholine Promotes Phagosome Maturation and Regulates Inflammatory Mediator Production Through the Protein Kinase A–Phosphatidylinositol 3 Kinase–p38 Mitogen-Activated Protein Kinase Signaling Pathway During Mycobacterium tuberculosis Infection in Mouse Macrophages

Lysophosphatidylcholine Promotes Phagosome Maturation and Regulates Inflammatory Mediator Production Through the Protein Kinase A–Phosphatidylinositol 3 Kinase–p38 Mitogen-Activated Protein Kinase Signaling Pathway During Mycobacterium tuberculosis Infection in Mouse Macrophages

Regulatory Effect of Cinnamaldehyde on Monocyte/Macrophage-Mediated Inflammatory Responses

Unique plasma metabolomic signature of osteonecrosis of the femoral head

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