Culture of mononuclear phagocytes on a teflon surface to prevent adherence.

Meer, J W van der; Bulterman, D; Zwet, T L van; Elzenga-Claasen, I; Furth, R. van

doi:10.1084/jem.147.1.271

Cited by 60 publications

(14 citation statements)

References 7 publications

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“…2A). Cultivation of monocyte preparations in Teflon beakers leads to differentiation into cells possessing a mature monocyte phenotype (27,28). During the maturation process, increased expression of PPAR␥ was observed ( Fig.…”

Section: Ppar␥ Agonists Do Not Inhibit Cytokine Production By Monocytmentioning

confidence: 99%

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Activation of Peroxisome Proliferator-Activated Receptor γ Does Not Inhibit IL-6 or TNF-α Responses of Macrophages to Lipopolysaccharide In Vitro or In Vivo

Thieringer¹,

Fenyk-Melody²,

Grand³

et al. 2000

The Journal of Immunology

184

115

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We have investigated the potential use of peroxisome proliferator-activated receptor γ (PPARγ) agonists as anti-inflammatory agents in cell-based assays and in a mouse model of endotoxemia. Human peripheral blood monocytes were treated with LPS or PMA and a variety of PPARγ agonists. Although 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) at micromolar concentrations significantly inhibited the production of TNF-α and IL-6, four other high affinity PPARγ ligands failed to affect cytokine production. Similar results were obtained when the monocytes were allowed to differentiate in culture into macrophages that expressed significantly higher levels of PPARγ or when the murine macrophage cell line RAW 264.7 was used. Furthermore, saturating concentrations of a potent PPARγ ligand not only failed to block cytokine production, but also were unable to block the inhibitory activity of 15d-PGJ2. Thus, activation of PPARγ does not appear to inhibit the production of cytokines by either monocytes or macrophages, and the inhibitory effect observed with 15d-PGJ2 is most likely mediated by a PPARγ-independent mechanism. To examine the anti-inflammatory activity of PPARγ agonists in vivo, db/db mice were treated with a potent thiazolidinedione that lowered their elevated blood glucose and triglyceride levels as expected. When thiazolidinedione-treated mice were challenged with LPS, they displayed no suppression of cytokine production. Rather, their blood levels of TNF-α and IL-6 were elevated beyond the levels observed in control db/db mice challenged with LPS. Comparable results were obtained with the corresponding lean mice. Our data suggest that compounds capable of activating PPARγ in leukocytes will not be useful for the treatment of acute inflammation.

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Section: Ppar␥ Agonists Do Not Inhibit Cytokine Production By Monocytmentioning

confidence: 99%

“…Culture of mononuclear phagocytes in suspension by incubation on a Teflon surface to which cells do not adhere has been described previously (27,28). Briefly, 1 ϫ 10 7 monocytes were resuspended in 10 ml of RPMI 1640 medium with L-glutamine and 14% normal human serum/60-ml Teflon beaker.…”

Section: Monocyte Culture Using Teflon Beakersmentioning

confidence: 99%

Activation of Peroxisome Proliferator-Activated Receptor γ Does Not Inhibit IL-6 or TNF-α Responses of Macrophages to Lipopolysaccharide In Vitro or In Vivo

Thieringer¹,

Fenyk-Melody²,

Grand³

et al. 2000

The Journal of Immunology

184

115

View full text Add to dashboard Cite

show abstract

“…BMM were obtained from mouse femurs and cultured in Teflon flasks (Dou et al 2006; van der Meer et al 1978). BMM were labeled with SPIO (Feridex, Berlex Inc., Wayne, NJ) by incubation with 2.5 mg/ml of Feridex/10 7 BMM/ml in complete media for 1 hour at 37°C (Zelivyanskaya et al 2003).…”

Section: Methodsmentioning

confidence: 99%

Ingress of blood-borne macrophages across the blood-brain barrier in murine HIV-1 encephalitis

Liu

Uberti

Dou

et al. 2008

Journal of Neuroimmunology

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Blood borne macrophage ingress into brain in HIV-1 associated neurocognitive disorders governs the tempo of disease. We used superparamagnetic iron-oxide particles loaded into bone marrowderived macrophages (BMM) injected intravenously into HIV-1 encephalitis mice to quantitatively assess BMM entry into diseased brain regions. Magnetic resonance imaging tests were validated by histological coregistration and enhanced image processing techniques. The demonstration of robust BMM migration into areas of focal encephalitis provide 'proof of concept' for the use of MRI to monitor macrophage migration into brain.

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“…An experimental approach has been devised that takes advantage of the ability of macrophages 1) to grow in suspension in Teflon flasks (Van der Meer et al, 1978) and 2) to adhere poorly to bacteriological petri dishes (Muschel et al, 1977). This procedure leads to low levels of basal adherence and thus allows quantification of the effect of modulators.…”

mentioning

confidence: 99%

“…In this study, we investigated the regulation of the adhesive capacity of the murine macrophage cell line 5-774 by cyclic adenosine monophosphate (CAMP)-dependent protein kinase (kinase A) and Ca2 + and phospholipid-dependent protein kinase (kinase C) activators. An experimental approach has been devised that takes advantage of the ability of macrophages 1) to grow in suspension in Teflon flasks (Van der Meer et al, 1978) and 2) to adhere poorly to bacteriological petri dishes (Muschel et al, 1977). This procedure leads to low levels of basal adherence and thus allows quantification of the effect of modulators.…”

mentioning

confidence: 99%

Biphasic regulation of macrophage attachment by activators of cyclic adenosine monophosphate‐dependent kinase and protein kinase C

Issaad

Ventura

Thomopoulos

1989

Journal Cellular Physiology

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A method is described that enabled us to study the adhesiveness of J-774 murine macrophages. Cell attachment was stimulated by activators of kinase C (i.e., phorbol esters) as well as kinase A (cyclic adenosine monophosphate; cAMP). This novel effect of cAMP was observed when its levels were increased via receptor triggering (prostaglandin E1, beta-adrenergic agonists), activation of Ns (cholera toxin), or inhibition of phosphodiesterase (Ro 20-1724) or when the kinase was directly activated by Br8-cAMP. The simultaneous treatment with kinase A and kinase C activators at the time of attachment resulted in a partially additive response. On the other hand, preincubation of the cells in suspension with one of the activators rendered them refractory to subsequent stimulation at the onset of the adhesion assay, whatever agent was used. Such a refractoriness was also observed in cells preincubated with oleoyl-acetyl-glycerol (OAG). On the other hand, when added at the time of attachment, this near-physiological activator of kinase C evoked a biphasic response: the early stimulation of cell attachment was followed by an accelerated rate of "detachment." In conclusion, kinase C and kinase A play a role in the sequence of events leading to cell adhesion. The cross desensitization observed is distal and takes place at or beyond the kinase step.

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Culture of mononuclear phagocytes on a teflon surface to prevent adherence.

Cited by 60 publications

References 7 publications

Activation of Peroxisome Proliferator-Activated Receptor γ Does Not Inhibit IL-6 or TNF-α Responses of Macrophages to Lipopolysaccharide In Vitro or In Vivo

Activation of Peroxisome Proliferator-Activated Receptor γ Does Not Inhibit IL-6 or TNF-α Responses of Macrophages to Lipopolysaccharide In Vitro or In Vivo

Ingress of blood-borne macrophages across the blood-brain barrier in murine HIV-1 encephalitis

Biphasic regulation of macrophage attachment by activators of cyclic adenosine monophosphate‐dependent kinase and protein kinase C

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