Circulating levels of both Th1 and Th2 chemokines are elevated in patients with sarcoidosis

Nureki, Shin-ichi; Miyazaki, Eishi; Ando, Masayuki; Ueno, Takamasa; Fukami, Tetsujiro; Kumamoto, Toshihide; Sugisaki, Katsunori; Tsuda, Toshihide

doi:10.1016/j.rmed.2007.09.006

Cited by 35 publications

(27 citation statements)

References 39 publications

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“…Ligands for these receptors are also increased, including MIP-1a/CCL3, MIP-1b/CCL4, MCP-1/CCL2, IFN-c inducible protein-10 (IP-10/CXCL10) and the chemokine 'Regulated on Activation, Normal T-cell Expressed and Secreted' (RANTES/CCL5) in BAL protein, peripheral blood (Iida et al 1997;Takeuchi et al 2006) and alveolar lymphocyte mRNA measurements (Petrek et al 2002) (Table 3). Contrastingly, expression of the T H 2 chemokines and the chemokine receptors CCR4 and CXCR4 is decreased in BAL fluid compared with peripheral blood T cells , whilst levels of both T H 1 and T H 2 chemokines and receptor expression appear to be elevated in peripheral blood of sarcoid patients (Nureki et al 2008). BAL fluid has high positive predictive values for the diagnosis of pulmonary sarcoidosis by detecting a lymphocytosis with elevated ratios of CD4?/CD8?…”

Section: Immunopathogenesis Of Sarcoidosismentioning

confidence: 90%

“…Also, strong responses were identified against lysyl tRNA synthetase and ATP synthase in BAL T cells of both DRB1*0301 positive and negative patients (Wahlström et al 2009). These suggest possible autoimmune responses in HLA-DRB1*0301 patients contributing to sarcoid granulomatous inflammation Immunological markers of sarcoidosis 59 chemokines and their receptors (Nureki et al 2008), which are highly expressed in the lungs of sarcoidosis patients (Moller 1999). Increased expression of T H 1 chemokine and cytokine receptors CXCR3, CCR5, IL-12R and IL-18R in sarcoid BAL fluid compared to peripheral blood CD4?…”

Section: Immunopathogenesis Of Sarcoidosismentioning

confidence: 99%

“…T cells compared with control subjects Nureki et al 2008), reflecting the systemic nature of sarcoidosis. The following discussion explores this debate.…”

Section: Ex Vivo Stimulation Of Lymphocytes From Blood and Bal Fluidmentioning

confidence: 99%

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The potential of the immunological markers of sarcoidosis in exhaled breath and peripheral blood as future diagnostic and monitoring techniques

2011

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Sarcoidosis is characterised by non-caseating granulomatous inflammation, with exaggerated immune responses at sites of disease and derangements of normal tissue architecture. The lungs are most commonly involved and progressive inflammation may result in pulmonary fibrosis. The immunopathogenesis and aetiology remain uncertain, which has made it difficult to identify a single sufficiently sensitive or specific diagnostic marker. Further investigation is needed to identify sensitive and specific markers of disease, such as in peripheral blood and exhaled breath condensate (EBC). Identification of disease markers may also be useful for investigating disease activity and predicting progression to fibrosis. This review explores the literature on the cytokine profiles of blood and bronchoalveolar lavage lymphocytes following ex vivo stimulation, as well as disease markers measured using the medium of EBC.

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Section: Immunopathogenesis Of Sarcoidosismentioning

confidence: 90%

Section: Immunopathogenesis Of Sarcoidosismentioning

confidence: 99%

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The potential of the immunological markers of sarcoidosis in exhaled breath and peripheral blood as future diagnostic and monitoring techniques

2011

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“…It could be hypothesized that CXCL10 may intensify or support a T cell-mediated inflammatory attack in MS. On the other hand, increased concentrations of the CXCL10 chemokine have been found in the CSF of patients with neuroborreliosis and tick-borne encephalitis [19,20] . The role of CXCL10 in sarcoidosis and Alzheimer disease is also under investigation [21,22] . These observations suggest that increased expression of CXCL10 is not specific for the demyelinating process in MS.…”

Section: Discussionmentioning

confidence: 99%

CCL5, CXCL10 and CXCL11 Chemokines in Patients with Active and Stable Relapsing-Remitting Multiple Sclerosis

Szczuciński¹,

Losy²

2010

Neuroimmunomodulation

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Objective: Chemokines are involved in the migration of inflammatory cells to the central nervous system in multiple sclerosis (MS). The aim of our study was to estimate the concentrations of CCL5, CXCL10 and CXCL11 in serum and cerebrospinal fluid (CSF) samples of relapsing-remitting MS (RRMS) patients during both relapse and stable disease, and to compare the results with those of controls. We also decided to evaluate the effect of methylprednisolone (MP) therapy on CCL5, CXCL10 and CXCL11 serum concentrations in MS patients with relapse. Methods: The study groups consisted of 17 RRMS patients during relapse, 30 RRMS patients in remission and 25 patients with tension headache with no symptoms of inflammatory disease as controls. In the group of relapsing MS patients, blood samples were obtained before steroid therapy and after a 5-day treatment with MP at a dose of 1 g i.v. once daily. Chemokine levels were measured by ELISA. Results: CXCL10 levels were significantly higher in the CSF of MS patients both during relapse (mean ± SD, 298.2 ± 143.8 pg/ml) and stable disease (323.7 ± 183 pg/ml) in comparison with the control group (152.4 ± 97.7 pg/ml; p < 0.001). CSF levels of CCL5 were significantly higher in relapsing MS patients (8.74 ± 6.18 pg/ml) in comparison with stable MS patients (4.4 ± 3.9 pg/ml, p = 0.005). CXCL11 levels of MS patients did not significantly differ from control values. There was no effect of MP therapy on serum levels of CCL5, CXCL10 and CXCL11. Conclusions: These observations suggest involvement of CXCL10 and CCL5 but not CXCL11 in the pathogenesis of MS. CCL5 may induce the recruitment of inflammatory cells in acute-stage MS.

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“…None of the patients and controls received corticosteroid therapy at the time of sample retrieval. The BAL procedure and a cell analysis were performed as described previously [18]. BAL was performed by injection of 150 ml of saline into the middle lobe or left lingula.…”

Section: Methodsmentioning

confidence: 99%

Elevated Concentrations of Liver-Expressed Chemokine/CC Chemokine Ligand 16 in Bronchoalveolar Lavage Fluid from Patients with Eosinophilic Pneumonia

Nureki

Miyazaki²,

Usagawa³

et al. 2009

Int Arch Allergy Immunol

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Background: Eosinophilic pneumonia is characterized by the prominent accumulation of eosinophils and lymphocytes in the lung parenchyma. Liver-expressed chemokine (LEC)/CC chemokine ligand 16 (CCL16) is a novel functional ligand for H4 which is expressed on eosinophils and also an affinity ligand for CCR1, CCR2, CCR5 and CCR8 which are expressed on T lymphocytes and monocytes. The purpose of this study is to clarify the role of LEC/CCL16 in eosinophilic pneumonia. Methods: The LEC/CCL16 level was measuredusing an enzyme-linked immunosorbent assay in the bronchoalveolar lavage fluid (BALF) of 33 patients with eosinophilic pneumonia, 26 patients with sarcoidosis and 10 healthy volunteers. The cell sources of LEC/CCL16 in BALF were evaluated by immunocytochemistry. Results: The LEC/CCL16 levels in BALF from patients with eosinophilic pneumonia were significantly higher than those from patients with sarcoidosis and healthy volunteers. The BALF LEC/CCL16 levels correlated with the numbers of BALF eosinophils and lymphocytes, respectively. The BALF LEC/CCL16 levels were significantly decreased after remission in eosinophilic pneumonia. In immunocytochemistry, the LEC/CCL16 expression was clearly observed in CD1a-positive dendritic cells as well as in CD68-positive macrophages harvested from patients with eosinophilic pneumonia, but not from the controls. Conclusions: These results suggest that LEC/CCL16 produced by dendritic cells as well as by alveolar macrophages contributes to the accumulation of eosinophils and lymphocytes into the inflamed lungs of patients with eosinophilic pneumonia.

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Circulating levels of both Th1 and Th2 chemokines are elevated in patients with sarcoidosis

Abstract: IP-10 is mainly produced at the lung and TARC in the peripheral circulation in sarcoidosis patients. Both IP-10 and TARC cooperatively play a role in the pathogenesis of sarcoidosis.

Cited by 35 publications

References 39 publications

The potential of the immunological markers of sarcoidosis in exhaled breath and peripheral blood as future diagnostic and monitoring techniques

The potential of the immunological markers of sarcoidosis in exhaled breath and peripheral blood as future diagnostic and monitoring techniques

CCL5, CXCL10 and CXCL11 Chemokines in Patients with Active and Stable Relapsing-Remitting Multiple Sclerosis

Elevated Concentrations of Liver-Expressed Chemokine/CC Chemokine Ligand 16 in Bronchoalveolar Lavage Fluid from Patients with Eosinophilic Pneumonia

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