Endothelin-induced activation of neutrophil migration

Elferink, J. G. R.; Koster, Ben M. de

doi:10.1016/0006-2952(94)90356-5

Cited by 59 publications

(31 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These findings suggest that ETA antagonists can inhibit neutrophil migration, a finding observed previously with BQ-123 and migration of rabbit neutrophils (Elferink and de Koster, 1994) and in neutrophil-driven ischemia in hearts with the selective antagonist LU135252 attenuating the neutrophilmediated injury (Andrasi et al, 2002). The importance of ETA antagonists in inhibiting inflammation has also been demonstrated in models of asthma with FR139317 inhibiting airway hyperresponsiveness (D'Agostino et al, 1999), lung eosinophilia (Fujitani et al, 1997), and paw edema (Sampaio et al, 1995).…”

Section: Discussionsupporting

confidence: 67%

“…They exert their effects in part by suppressing the release of chemotactic agents and reducing adhesion molecule expression, ultimately leading to inhibition of neutrophil accumulation. This study has been prompted by the observation that ET-1 led to the migration of rabbit neutrophils (Elferink and de Koster, 1994). However, we now report here for the first time that ET-1 antagonists are efficacious in a murine model of gouty peritonitis.…”

Section: Discussionmentioning

confidence: 75%

“…The involvement of ET-1 in inflammatory pathologies has been documented, including arthritic pathologies (Yoshida et al, 1998), with detection in human synovial tissue (Wharton et al, 1992), whereas increased production of ET-1 occurs in the synovial fluid compared with plasma in patients with inflammatory arthritides (Miyasaka et al, 1992), a fact confirmed more recently in rheumatoid arthritic patients (Haq et al, 1999) and arthritic joints (Gutierrez et al, 1996). ET-1 release has long been known to lead to neutrophil migration in rabbits (Elferink and de Koster, 1994) and to cause neutrophil-driven ischemia in hearts (Andrasi et al, 2002). An efficacy with antagonists directed at the ET-1 receptors at inhibiting inflammation has also been demonstrated in models of asthma with FR139317 inhibiting airway hyperresponsiveness (D'Agostino et al, 1999), lung eosinophilia (Fujitani et al, 1997), and paw edema (Sampaio et al, 1995).…”

mentioning

confidence: 92%

See 2 more Smart Citations

Investigation into the Potential Anti-Inflammatory Effects of Endothelin Antagonists in a Murine Model of Experimental Monosodium Urate Peritonitis

Getting¹,

Filippo²,

Lam³

et al. 2004

J Pharmacol Exp Ther

View full text Add to dashboard Cite

Endothelin (ET)-1 has been detected in many inflammatory pathologies, including rheumatoid arthritic patients, asthma, and ischemic-reperfusion injury. In this study, we have investigated the effect of a panel of different ET-1 antagonists displaying different selectivities for the receptors in a murine model of experimental inflammatory peritonitis. Systemic treatment of mice with the ETA antagonist C 33 H 44 N 6 O 5 , N-[N-[-N(hexahydro-1H-azepin- all these effects occurred without altering peripheral blood cell counts. Release of the CXC chemokine KC was significantly reduced by the FR139317 and PD145065 but not by BQ-788. Evaluation of the therapeutic potential of these antagonists showed that PD145065 inhibited neutrophil migration and KC release, whereas the others caused a nonsignificant reduction in these parameters. Parameters of endothelial cell activation showed that urate-stimulated interleukin-1␤ release was inhibited by BQ-788 and PD145065 but not by FR139317, whereas ET-1 was only inhibited by the mixed antagonist. A different scenario was observed with respect to release of the CXC chemokine KC with FR139317 and PD145065 being effective, whereas with a marker of polymorphonuclear activation the ETA and mixed antagonist inhibited adhesion molecule expression. These data show that ET-1 antagonists elicit different mechanisms of actions in the way they display their antimigratory effects in a murine model of monosodium urate crystal peritonitis.Monosodium urate (MSU) crystal deposition into the joint articular space is responsible for the inflammatory condition known as gouty arthritis (McCarty et al., 1962). Edema and erythema of the joints with severe pain and infiltration of polymorphonuclear (PMN) leukocytes are associated with this pathology (Dieppe et al., 1979;Terkeltaub, 1992). MSU crystals cause the synthesis of CXC chemokines selective for PMN, such as murine KC (Getting et al., 1997) but not that of a CC chemokine selective for monocytes, such as monocyte chemoattractant protein-1 (Hachicha et al., 1995), a scenario that will lead to PMN but not monocyte migration. In addition, MSU crystal activation of intra-articular mononuclear phagocytes also induces secretion of interleukin-8 (Terkeltaub et al., 1991). All these studies provide further evidence that gouty arthritis is mainly a PMN-driven pathology. Murine KC shows a 60% homology to human growth-related oncogene-␣, and this chemokine has been shown to be selective for the human CXCR2. In mice, only the CXCR2 exists, whereas in humans both CXCR2 and CXCR1 are present. KC binds to the murine CXCR2, and this has been shown to play a major role in neutrophil chemotaxis. Studies have shown that mice lacking the CXCR2 have fewer neutrophils infil-

show abstract

Section: Discussionsupporting

confidence: 67%

Section: Discussionmentioning

confidence: 75%

mentioning

confidence: 92%

See 1 more Smart Citation

Investigation into the Potential Anti-Inflammatory Effects of Endothelin Antagonists in a Murine Model of Experimental Monosodium Urate Peritonitis

Getting¹,

Filippo²,

Lam³

et al. 2004

J Pharmacol Exp Ther

View full text Add to dashboard Cite

show abstract

“…Thus, ET-1 tive, dP/dt, were continuously recorded on a polygraph stimulates aggregation of human PMNs [18], increases (Model 7D, Grass Instruments, USA). Coronary flow was PMN intracellular free calcium mobilisation [19,20] and measured by collecting the effluent, and heart rate was superoxide anion production by PMNs [21]. ET-1 stimudetermined from the pressure registration every 5 min.…”

Section: Introductionmentioning

confidence: 99%

The endothelin A receptor antagonist LU 135252 protects the myocardium from neutrophil injury during ischaemia/reperfusion

Gonon

Wang

Pernow

1998

Cardiovascular Research

View full text Add to dashboard Cite

Objective: Endothelin-1 (ET-1) is not only a potent vasoconstrictor but also a stimulator of polymorphonuclear leukocyte (PMN) aggregation and adhesion. The aim of this study was to investigate whether an ET receptor antagonist attenuates the PMN-mediated A contractile dysfunction following myocardial ischaemia. Methods: Isolated rat hearts were perfused according to the Langendorff method. The hearts were subjected to global ischaemia and reperfused with buffer solution only, or human PMNs dissolved in rat plasma (HNRP). Results:In an initial study, the ET receptor antagonist LU 135252 (1 and 10 mmol / l) or ET-1 (1 and 10 nmol / l) did not significantly A affect the recovery of left ventricular developed pressure (LVDP), end-diastolic pressure (LVEDP), the first derivative of left ventricular pressure (dP/dt) or the rate pressure product (RPP) during reperfusion with buffer solution only compared to a vehicle group. In a second study on hearts reperfused with HNRP, administration of LU 135252 (10 mmol / l) significantly enhanced the recovery of LVDP, dP/dt and RPP in hearts reperfused with HNRP. LVEDP was 20 mmHg lower in hearts given LU 135252 than vehicle in combination with HNRP (P,0.05). The outflow of PMNs in the coronary effluent during reperfusion was 4168% in hearts given LU 135252 compared to 965% in vehicle-treated hearts (P,0.01). There was a significant correlation between the myocardial functional recovery and the outflow of PMNs. Administration of ET-1 (0.1 and 1 nmol / l) in combination with HNRP resulted in complete loss of contractile function and no outflow of PMNs during reperfusion. Conclusion: The ET receptor antagonist LU 135252 protects from ischaemia / reperfusion injury in A the isolated rat heart in the presence of PMNs. It is suggested that inhibition of PMN-induced injury during reperfusion is an important cardioprotective action of LU 135252.

show abstract

“…Migration of neutrophils from the intravascular compartment to an inflammed tissue requires interaction of neutrophils with vascular endothelium and the presence of chemoattractants which serve as homing triggers. ET-1 upregulates the expression of adhesive molecules, CD18 and CD11b on neutrophil surface, and enhances neutrophil adhesion to pulmonary endothelium [9,11,17]. The findings of an elevated serum ET-1 in P. aeruginosa-infected patients, but not the other pro-inflammatory cytokines, suggests an important role for ET-1 in the endothelial recruitment of neutrophils in bronchiectasis.…”

Section: Discussionmentioning

confidence: 99%

Endothelin-1 in stable bronchiectasis

Zheng¹,

Tipoe²,

Lam³

et al. 2000

Eur Respir J

View full text Add to dashboard Cite

Endothelin (ET)-1 has been suggested to promote neutrophil adhesion to endothelium, migration to inflamed areas, and release of elastase. ET-1 might therefore play a role in the pathogenesis of bronchiectasis, a chronic inflammatory and infective airway disease which is still poorly understood.Thirty five patients with stable bronchiectasis (20 females, mean age SD 49.1 15.0 yrs) and 18 control subjects (8 females, 49.4 11.3 yrs) were recruited prospectively. The ET-1 levels in serum and sputum were measured by commercially available enzyme linked immunosorbent assay (ELISA) kits.Patients with Pseudomonas aeruginosa in their sputum had a significantly higher serum level of ET-1 (median 25.8, interquartile range 13±43.9 pg . mL -1 ) than patients without P. aeruginosa (0, 0±10.5 pg . mL -1 ; p=0.0004) and healthy control subjects (4.6, 0±16.3 pg . mL -1 ; p=0.002). However, patients with and without P. aeruginosa infection had no significant difference in sputum ET-1 level (p=0.15). There was no correlation between serum or sputum ET-1 levels with the serum and sputum levels of the interleukin (IL)-1b, IL-8 and tumour necrosis factor (TNF)-a; the number of bronchiectasis lung lobes; and spirometry. Serum ET-1 level correlated with 24 h sputum volume for the bronchiectasis patients (r=0.51, p=0.002).The results, therefore, suggest a significant pathogenic role for endothelin-1 among Pseudomonas aeruginosa-infected patients with bronchiectasis. Further studies should be performed to evaluate the clinico-pathological correlation and expression of endothelin-1 in bronchiectasis.

show abstract

Endothelin-induced activation of neutrophil migration

Cited by 59 publications

References 16 publications

Investigation into the Potential Anti-Inflammatory Effects of Endothelin Antagonists in a Murine Model of Experimental Monosodium Urate Peritonitis

Investigation into the Potential Anti-Inflammatory Effects of Endothelin Antagonists in a Murine Model of Experimental Monosodium Urate Peritonitis

The endothelin A receptor antagonist LU 135252 protects the myocardium from neutrophil injury during ischaemia/reperfusion

Endothelin-1 in stable bronchiectasis

Contact Info

Product

Resources

About