Neutrophil adhesion to histamine stimulated cultured endothelial cells is primarily mediated via activation of phospholipase C and nitric oxide synthase isozymes

Schaefer, U.; Schneider, Anja; Rixen, Dieter; Neugebauer, E.

doi:10.1007/s000110050327

Cited by 24 publications

(19 citation statements)

References 47 publications

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“…Consistent with these reports, we found that cimetidine, an H 2 -histamine receptor antagonist, abolished the increased expresion of PDE4B induced by histamine whilst dexchlorpheniramine, an H 1 -antihistamine, was not effective. H 3 -histamine receptor antagonists were not tested since the existence of this class of histamine receptors on human neutrophils seems unlikely [43,44] In addition, we examined whether the up-regulation by histamine of PDE4 activity in human neutrophils had an impact on their functional responsiveness to a different autacoid, PGE 2 , which also acts by increasing cAMP in human neutrophils following stimulation of EP 2 receptors coupled to adenylyl cyclase [45]. As demonstrated in concentrationresponse studies, pretreatment of cells with histamine substantially decreased the ability of PGE 2 to inhibit the SOZ-induced release of superoxide anion.…”

Section: Discussionmentioning

confidence: 99%

Histamine up-regulates phosphodiesterase 4 activity and reduces prostaglandin E 2 -inhibitory effects in human neutrophils

Dası́

Ortiz

Cortijo

et al. 2000

Inflammation Research

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Section: Discussionmentioning

confidence: 99%

Histamine up-regulates phosphodiesterase 4 activity and reduces prostaglandin E 2 -inhibitory effects in human neutrophils

Dası́

Ortiz

Cortijo

et al. 2000

Inflammation Research

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“…Isolation of neutrophils was performed as previously reported (Schaefer et al, 1998) with a slight modification. In short, 24 ml of venous blood was drawn, by venipuncture, from healthy donors into vacutainer tubes (Becton Dickinson, Plymouth, UK) containing 0.11 M sodium citrate and centrifuged at 1500 g for 5 min.…”

Section: Isolation and Preparation Of Calcein-labelled Human Neutrophilsmentioning

confidence: 99%

The new cardioprotector Monohydroxyethylrutoside protects against doxorubicin-induced inflammatory effects in vitro

et al. 2003

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Besides its cardiotoxic effect, doxorubicin also elicits inflammatory effects in vivo. 7-Monohydroxyethylrutoside (monoHER) has recently been used as a protector against doxorubicin-induced cardiotoxicity in vivo. It is not known yet whether monoHER can also protect against doxorubicin-induced inflammatory effects. The aim of the present study was (1) to illustrate the inflammatory effects of doxorubicin in vitro and (2) to evaluate a possibly protective effect of monoHER. In order to demonstrate the inflammatory effects of doxorubicin and the possible protection of monoHER, proliferating human umbilical cord vascular endothelial cells (HUVECs) were incubated with different concentrations of doxorubicin ranging from 12.5 to 600 nM with(out) 200 mM monoHER. Resting (confluent) HUVECs were incubated with (0.5 -25 mM) doxorubicin with(out) monoHER (0.2 -1.2 mM) and the viability of endothelial cells and their propensity to adhere to neutrophils were measured 24 h after treatment. The localisation of adhered neutrophils was determined with immunofluorescence microscopy. To further characterise the mechanism of doxorubicin-induced neutrophil adhesion, the expression of the HUVECs surface adhesion molecules was determined after doxorubicin treatment. Doxorubicin decreased the viability and proliferation capacity of HUVECs in a concentration-dependent manner. The proliferating HUVECs were much more sensitive to doxorubicin (IC 50 ¼ 60.0720.8 nM) than resting cells (LC 50 ¼ 4.070.3 mM). Doxorubicin also increased the adhesion of neutrophils reaching a plateau value at a doxorubicin concentration of X0.4mM (P ¼ 0.0113). The induced neutrophil adhesion was accompanied by overexpression of VCAM and E-selectin but not ICAM. Although monoHER did not reverse the effect of doxorubicin on the proliferation of endothelial cells, it significantly protected resting HUVECs against the cytotoxic effect of doxorubicin (p25 mM, Po0.0015). In addition, monoHER completely protected against the stimulatory effect of doxorubicin on neutrophil adhesion, and inhibited the doxorubin-induced expression of VCAM and E-selectin on the surface of treated HUVECs. This study illustrates that monoHER, which protects against doxorubicin's cardiotoxic effect, can also protect against doxorubicin-induced inflammatory effects. These data prompt further investigation about the possible link between doxorubicin-induced inflammatory effects and its cardiotoxicity in vivo.

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“…res. 53 (2004) 223 -229 1023-3830/04/060223-07 DOI 10.1007/s00011-004-1246-4 trophil adhesion to endothelial cells [8,9]. These effects have been shown to be mediated by the binding of histamine to specific G-protein-coupled cell surface receptors (GPCR), designated H 1 to H 4 [10][11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Polyclonal anti-histamine H 2 receptor antibodies detect differential expression of H 2 receptor protein in primary vascular cell types

Schneider

Rieß

Elbers

et al. 2004

Inflammation Research

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We conclude that the antibodies generated against the extra-cellular domain of the H2 receptor are specific and can be utilized to detect and quantify H2 receptor expression. Furthermore, the significant differences in H2 receptor expression in different vascular cell types might play a critical role in defining histamine induced cellular responses during physiological or pathophysiological processes.

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Neutrophil adhesion to histamine stimulated cultured endothelial cells is primarily mediated via activation of phospholipase C and nitric oxide synthase isozymes

Abstract: Our results suggest that histamine stimulated neutrophil adhesion is due to H1 and H2 receptor mediated activation of PLC, NOS and GC. Increase of cAMP concentration seems to mediate an inhibitory effect on PMN adhesion to endothelial cells.

Cited by 24 publications

References 47 publications

Histamine up-regulates phosphodiesterase 4 activity and reduces prostaglandin E 2 -inhibitory effects in human neutrophils

Histamine up-regulates phosphodiesterase 4 activity and reduces prostaglandin E 2 -inhibitory effects in human neutrophils

The new cardioprotector Monohydroxyethylrutoside protects against doxorubicin-induced inflammatory effects in vitro

Polyclonal anti-histamine H 2 receptor antibodies detect differential expression of H 2 receptor protein in primary vascular cell types

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