Systemic inflammation in COPD visualised by gene profiling in peripheral blood neutrophils

Oudijk, Erik-Jan; Nijhuis, Evert; Zwank, M. D.; Graaf, E.A. van de; Mager, Hans‐Jurgen; Coffer, Paul J.; Lammers, Jan-Willem; Koenderman, Leo

doi:10.1136/thx.2004.034009

Cited by 76 publications

(65 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For human GAPDH a 135-bp fragment was amplified using the FW primer 5Ј-AGAAGGCTGGGGCTCA-TTT-3Ј and RV primer 5Ј-GAGGCATTGCTGATGATC-TTG-3Ј, and a 174-bp fragment of ␤-actin was amplified using FW primer 5Ј-AGCCTCGCCTTTGCCGA-3Ј and RV primer 5Ј-CTGGTGCCTGGGGCG-3Ј (32). The real-time PCR was performed as previously described (31). Results were normalized for the housekeeping genes ␤-actin and GAPDH, and results were expressed as -fold regulation.…”

Section: Methodsmentioning

confidence: 99%

“…5 ϫ 10 6 cells were harvested, washed twice with phosphate-buffered saline, lysed in 1 ml of TRIzol (Invitrogen), and stored at Ϫ20°C. Total cellular RNA was isolated, and cDNA was generated as previously described (31) according to the manufacturer's protocol (Invitrogen). 10 g of RNA was treated with DNase according to the manufacturer's protocol (DNAfree, Ambion Inc., Austin, TX).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

FOXO3a Induces Differentiation of Bcr-Abl-transformed Cells through Transcriptional Down-regulation of Id1

Birkenkamp

Essafi

Vos

et al. 2007

Journal of Biological Chemistry

View full text Add to dashboard Cite

Homeostasis of the hematopoietic system requires tight control of proliferation, differentiation, and survival of progenitor cells (1-5). Combinations of cytokines acting on a progenitor cell initiate a specific developmental program through activation of distinct downstream signal-transduction pathways (6).Interference with this highly regulated process can lead to the development of hematopoietic malignancies. Myeloid transformation is often associated with chromosomal translocations and somatic mutations, affecting gene expression in ways that lead to defects in normal programs of cell proliferation, differentiation, and survival (7-12). For instance, chronic myeloid leukemia (CML) 9 is a lethal hematopoietic stem cell malignancy characterized by the t(9,22) chromosomal translocation, a translocation between the long arms of chromosomes 9 and 22, resulting in the formation of the Philadelphia (ph) chromosome and the fusion of a truncated bcr gene to the 5Ј-upstream sequences of the second exon of c-abl (9, 13). The bcr-abl fusion gene is known to be essential to the pathogenesis of CML, and the Bcr-Abl protein demonstrates constitutively active kinase activity, which is essential and sufficient for malignant transformation (9, 13, 14). Bcr-Abl exerts diverse actions on hematopoietic cells in terms of cellular transforming activity, inhibition of apoptosis, cell cycle progression, altered cell migration, and adhesion to extracellular matrix (9, 13, 14). Expression of Bcr-Abl results in growth factor independence of cells and activates multiple signaling cascades, including the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB/c-Akt) signaling pathway (15,16).In non-malignant cells activation of the PI3K/PKB-signaling module is stimulated by growth factors and cytokines and has been linked to regulation of cellular proliferation and survival in a diverse variety of cell systems (17)(18)(19). Recently, it has been demonstrated that the members of the FOXO subfamily of transcription factors FOXO1, FOXO3a, and FOXO4 are directly phosphorylated by PKB (20,21). In the absence of growth or survival factors FOXOs are unphosphorylated, localized in the nucleus, and transcriptionally active. Upon stimulation with growth factors or cytokines, PKB activity is induced, and it translocates to the nucleus and phosphorylates FOXOs, leading to inhibition of transcriptional activity and nuclear export (22). We and others have demonstrated that FOXO transcription factors can regulate a variety of genes that influence cellular proliferation (e.g. p27 Kip1 and cyclin D), survival * This work was supported in part by the Dutch Scientific Organization (Grant NWO-90128139). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. 31-30-250-4305; E-mail: P.J.Coffer@umcutrecht.nl. 9 The abbreviations used are: CML, chronic myeloid leukemia; PEPCK, phosphoenolpyruvate carboxykinase; PI3K, phosphatidyli...

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

FOXO3a Induces Differentiation of Bcr-Abl-transformed Cells through Transcriptional Down-regulation of Id1

Birkenkamp

Essafi

Vos

et al. 2007

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…As neutrophils (PMN) are a major cell type involved in COPD (Cowburn et al, 2008;Nathan, 2006;Oudijk et al, 2005;Quint & Wedzicha, 2007), this could imply PMN-dominated inflammatory processes also characterize many SM-related lung pathologies.…”

Section: Introductionmentioning

confidence: 99%

Comparative proteome analysis of peripheral neutrophils from sulfur mustard-exposed and COPD patients

Shahriary

Mehrani

Ghanei

et al. 2014

Journal of Immunotoxicology

View full text Add to dashboard Cite

Respiratory disorders in sulfur mustard (SM)-exposed and chronic obstructive pulmonary disease (COPD) patients are mostly associated with neutrophilic inflammation, severe airflow limitation, and oxidative stress. The objective of this study was to establish whether neutrophil (PMN) proteomes in these diseases were similar or differed. Blood neutrophil proteomes from healthy, SM-exposed, and COPD subjects were analyzed using two-dimensional gel electrophoresis followed by matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI TOF MS). Elastase activity was determined kinetically. The results showed that levels of S100 calcium-binding protein (CBP) A12, S100 CBP A8, glyceraldehyde-3-phosphate dehy-drogenase, superoxide dismutase, and protein disulfide isomerase proteinsas well as elastase activity -were significantly increased in PMN from 'diseased' hosts compared to in cells from healthy controls. In contrast, coactosin-like protein, RhoGDP dissociation inhibitor, and actin isoforms were significantly decreased in diseased subjects' PMN compared to PMN of healthy controls. Moreover, serpin B1 and coronin-1A were expressed only in PMN of the healthy subjects. Lastly, S100 CBP A9, endoplasmic reticulum (ER)-60 protease, and glutathione-S-transferase isoforms were differentially expressed in the cells from the SMexposed and COPD subjects. These results show that serpin B1, an efficient inhibitor of neutrophil serine proteases, was not detectable, and elastase activity significantly increased in PMN from both SM-exposed and COPD patients. It seems that, apart from inflammation and oxidative stress, a protease:anti-protease imbalance exists within PMN of both COPD and SM-exposed patients.

show abstract

“…Granulocytes were isolated from 100 ml whole blood of healthy donors as described before (Oudijk et al, 2005). Negative immunomagnetic selection was used to purify eosinophils from granulocytes using anti-CD16-conjugated microbeads (Miltenyi Biotec; Auburn, CA) (Hansel et al, 1991).…”

Section: Granulocyte Isolation and Stimulationmentioning

confidence: 99%

“…The cytokines TNF␣ and GM-CSF were investigated in these processes because they use distinct receptors that are expressed on both cell types. In addition, both cytokines have been associated with chronic inflammation in inflammatory diseases, such as asthma and COPD (Oudijk et al, 2003(Oudijk et al, , 2005Thomas, 2001;Ritz et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Differential regulation of TNFα and GM-CSF induced activation of P38 MAPK in neutrophils and eosinophils

Hove

Houben

Raaijmakers

et al. 2007

Molecular Immunology

View full text Add to dashboard Cite

P38 MAPK is a central mediator in cytokine signalling in human leukocytes. P38 MAPK is activated by phosphorylation of a conserved Thr180-X-Tyr182 motif by dual phosphorylation via the upstream kinases MKK3 and MKK6. Alternatively, P38 MAPK can be activated via autophosphorylation when associated with TAB1. In this study P38 MAPK phosphorylation and activation (measured via phosphorylation of P38 MAPK downstream target MK2) were investigated upon engagement of the GM-CSF-and TNF␣-receptors expressed on both eosinophils and neutrophils. The MKK3/MKK6 pathway mediated neutrophil P38 MAPK activation after stimulation with TNF␣ (100 U/ml) or GM-CSF (10 −10 M). Under these conditions the activation but not phosphorylation of P38 MAPK could be inhibited by SB203580 (10 −5 M or 10 −6 M). In eosinophils SB203580 (10 −6 M) inhibited both the phosphorylation and activation of P38 MAPK after stimulation with several doses of TNF␣ (10-10000 U/ml) or GM-CSF (10 −11 to 10 −9 M), indicating that P38 MAPK activation is mediated via autophosphorylation in eosinophils. This hypothesis was supported by the finding that in marked contrast to neutrophils, MKK3/MKK6 did not show enhanced phosphorylation in eosinophils after cytokine stimulation, but were constitutively phosphorylated. Therefore, the involvement of TAB1 was investigated with regard to this cytokine-induced autophosphorylation. Co-immunoprecipitation experiments showed that TAB1 was constitutively associated with P38 MAPK in eosinophils and neutrophils and that cytokine-induced autophosphorylated P38 MAPK was co-precipitated with TAB1. These findings are consistent with the hypothesis that cytokine-induced autophosphorylation of P38 MAPK in primary granulocytes depends on the interaction with TAB1.

show abstract

Systemic inflammation in COPD visualised by gene profiling in peripheral blood neutrophils

Cited by 76 publications

References 29 publications

FOXO3a Induces Differentiation of Bcr-Abl-transformed Cells through Transcriptional Down-regulation of Id1

FOXO3a Induces Differentiation of Bcr-Abl-transformed Cells through Transcriptional Down-regulation of Id1

Comparative proteome analysis of peripheral neutrophils from sulfur mustard-exposed and COPD patients

Differential regulation of TNFα and GM-CSF induced activation of P38 MAPK in neutrophils and eosinophils

Contact Info

Product

Resources

About