Glucocorticoids inhibit chemokine generation by human eosinophils

Miyamasu, Misato; Misaki, Yoshikata; Izumi, Satoshi; Takaishi, Toshiaki; Morita, Yutaka; Nakamura, Haruji; Matsushima, Kouji; Kimura, Tadashi; Hirai, Koichi

doi:10.1016/s0091-6749(98)70196-4

Cited by 58 publications

(45 citation statements)

References 27 publications

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“…Smith and Herschman (20) identified cDNAs for seven LPS-induced genes for chemokines that were attenuated by glucocorticoid, including MCP-1. Several authors have demonstrated that dexamethasone inhibits MCP-1 gene expression by various cell populations; including airway smooth muscle cells (45), eosinophils (46), and PBMC (47). In addition, dexamethasone treatment decreased MCP-1 mRNA expression and protein release in the peritoneal fluid in IL-1-stimulated mice (48).…”

Section: Discussionmentioning

confidence: 99%

Role of Monocyte Chemotactic Protein-1/CC Chemokine Ligand 2 on γδ T Lymphocyte Trafficking during Inflammation Induced by Lipopolysaccharide orMycobacterium bovisBacille Calmette-Guérin

Penido

Vieira‐de‐Abreu

Bozza

et al. 2003

The Journal of Immunology

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γδ T lymphocytes are involved in a great variety of inflammatory and infectious responses. However, the mechanisms by which γδ T lymphocytes migrate to inflamed sites are poorly understood. In this study we investigate the role of monocyte chemotactic protein (MCP)-1 in regulating γδ T cell migration after LPS or Mycobacterium bovis bacille Calmette-Guérin (BCG) challenge. LPS-induced γδ T cell influx was significantly inhibited by either pretreatment with dexamethasone or vaccinia virus Lister 35-kDa chemokine binding protein, vCKBP, a CC chemokine neutralizing protein, suggesting a role for CC chemokines in this phenomenon. LPS stimulation increased the expression of MCP-1 mRNA and protein at the inflammation site within 6 h. It is noteworthy that LPS was unable to increase MCP-1 production or γδ T cell recruitment in C3H/HeJ, indicative of the involvement of Toll-like receptor 4. γδ T cells express MCP-1 receptor CCR2. Pretreatment with anti-MCP-1 mAb drastically inhibited LPS-induced in vivo γδ T cell mobilization. Indeed, MCP-1 knockout mice were unable to recruit γδ T cells to the pleural cavity after LPS stimulation, effect that could be restored by coadministration of MCP-1. In addition, BCG-induced γδ lymphocyte accumulation was significantly reduced in MCP-1 knockout mice when compared with wild-type mice. In conclusion, our results indicate that LPS-induced γδ T lymphocyte migration is dependent on Toll-like receptor 4 and sensitive to both dexamethasone and CC chemokine-binding protein inhibition. Moreover, by using MCP-1 neutralizing Abs and genetically deficient mice we show that LPS- and BCG-induced γδ T lymphocyte influx to the pleural cavity of mice is mainly orchestrated by the CC chemokine MCP-1.

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Section: Discussionmentioning

confidence: 99%

Role of Monocyte Chemotactic Protein-1/CC Chemokine Ligand 2 on γδ T Lymphocyte Trafficking during Inflammation Induced by Lipopolysaccharide orMycobacterium bovisBacille Calmette-Guérin

Penido

Vieira‐de‐Abreu

Bozza

et al. 2003

The Journal of Immunology

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“…After precipitation with ethanol, the first-strand cDNA was reverse transcribed as described previously. 46 The second-strand DNA synthesis and hotstart amplification were performed using a thermal cycler (Thermal cycler MP, Takara, Kyoto, Japan).…”

Section: Chemotaxis Analysis Of Ccr3 Chemoattractant To Eosinophilsmentioning

confidence: 99%

“…Amplification of cDNA was performed as previously described 46 except that AmpliTaq Gold DNA polymerase (Perkin-Elmer, Branchburg, NJ, USA) was used. Direct and reverse oligo primers for CCR3 (5′-ATCCTACTAT GATGACGTGGGC-3′; position TM1 for sense and 5′-GGCCAGGTACCTGTCGATTG-3′; position TM3 for antisense) were constructed based on the published sequences of mRNA.…”

Section: Chemotaxis Analysis Of Ccr3 Chemoattractant To Eosinophilsmentioning

confidence: 99%

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New variations of human CC-chemokine receptors CCR3 and CCR4

et al. 1999

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CCR3 and CCR4 are the members of CC chemokine receptor family expressed on Th2 type CD4 + T cells. In this study, variation screening of the entire coding regions of CCR3 and CCR4 was performed, and possible association with several autoimmune diseases was tested, using the genomic DNA from 304 Japanese healthy individuals and 272 Japanese patients with rheumatic diseases. One non-synonymous substitution was identified in CCR3 gene, whereas in CCR4 gene, two non-synonymous and two synonymous substitutions were detected. Among the synonymous substitutions, CCR4 1014(C→T) was observed in 7.2% of the healthy individuals and 6.6% of the patients, and was considered as a single nucleotide polymorphism. All other variations were observed in only one or two individuals. No significant association was observed between any of the variations and any of the rheumatic diseases. Among these variations, CCR3-C218S substitution coded by 652(T→A) substitution was localized in the region conserved among the G protein coupled receptor family. Reactivity of eosinophils to the monoclonal antibody against CCR3 and the chemotaxis to eotaxin were slightly reduced in this patient as compared with healthy controls or a patient with Behçet disease homozygous for the common allele, while CCR3 mRNA level was not different. These findings suggest that CCR3-C218S substitution may lead to the reduced function of CCR3 at the protein level. Further study will be of interest to test whether CCR3-C218S variation or any of the CCR4 variations has a significant role in rendering susceptibility to immunological diseases or resistance to HIV infection.

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“…GCs have been widely used to treat several cancers, such as leukemias, lymphomas, and multiple myelomas; to treat rheumatic disorders, such as rheumatoid arthritis and systemic lupus erythematosus; to treat acute allergic conditions, such as drug hypersensitivity reactions, allergic dermatitides, and asthma; in transplant recipients to prevent acute transplant rejection and graft-versus-host disease; and to treat inflammatory diseases of the skin, bowel, and nervous system. GCs are potent inhibitors of MCP-1 synthesis in a variety of cell types (21,32,36,54), including SMCs (44)(45)(46)(47). GCs are reported to suppress intimal hyperplasia (6,55) and atherosclerosis (3,43).…”

mentioning

confidence: 99%

Y-Box Binding Protein 1 and RNase UK114 Mediate Monocyte Chemoattractant Protein 1 mRNA Stability in Vascular Smooth Muscle Cells

Dhawan

Liu

Pytlak

et al. 2012

Molecular and Cellular Biology

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Monocyte chemoattractant protein 1 (MCP-1) plays a pivotal role in many inflammatory processes, including the progression of atherosclerosis and the response of the arterial wall to injury. We previously demonstrated that dexamethasone (Dex) inhibits MCP-1 mRNA accumulation in smooth muscle cells by decreasing its half-life. The effect of Dex was dependent upon the glucocorticoid receptor (GR) and independent of new transcription. Using RNA affinity and column chromatography, we have identified two proteins involved in regulating MCP-1 mRNA stability: Y-box binding protein 1 (YB-1), a multifunctional DNA/RNA-binding protein, and endoribonuclease UK114 (UK). By immunoprecipitation, YB and GR formed a complex present in equal amounts in extracts from untreated and Dex-treated cells. YB-1, UK, and GR small interfering RNA (siRNA) substantially inhibited the effect of Dex on MCP-1 mRNA accumulation. In addition, YB-1 antibody blocked the degradation of MCP-1 mRNA by cytoplasmic extracts from the Dex-treated cells. The degradative activity of extracts immunoprecipitated with antibodies to either YB-1 or GR was blocked with UK antibody. UK did not degrade MCP-1 mRNA; however, upon addition to nondegrading control extracts, it rapidly degraded MCP-1 mRNA. These studies define new roles for GR, YB-1, and UK in the formation of a molecular complex that degrades MCP-1 mRNA.

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Glucocorticoids inhibit chemokine generation by human eosinophils

Cited by 58 publications

References 27 publications

Role of Monocyte Chemotactic Protein-1/CC Chemokine Ligand 2 on γδ T Lymphocyte Trafficking during Inflammation Induced by Lipopolysaccharide orMycobacterium bovisBacille Calmette-Guérin

Role of Monocyte Chemotactic Protein-1/CC Chemokine Ligand 2 on γδ T Lymphocyte Trafficking during Inflammation Induced by Lipopolysaccharide orMycobacterium bovisBacille Calmette-Guérin

New variations of human CC-chemokine receptors CCR3 and CCR4

Y-Box Binding Protein 1 and RNase UK114 Mediate Monocyte Chemoattractant Protein 1 mRNA Stability in Vascular Smooth Muscle Cells

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