0000000000373932

AUTHOR

Yafa Naim Abu Nabah

showing 11 related works from this author

A critical role for TNFα in the selective attachment of mononuclear leukocytes to angiotensin-II-stimulated arterioles

2007

Abstract Angiotensin II (Ang-II) exerts inflammatory activity and is involved in different cardiovascular disorders. This study has evaluated the involvement of tumor necrosis factor alpha (TNFα) in the leukocyte accumulation elicited by Ang-II. Ang-II (1 nM intraperitoneally in rats) induced TNFα release at 1 hour followed by neutrophil and mononuclear cell recruitment. The administration of an antirat TNFα antiserum had no effect on Ang-IIinduced neutrophil accumulation but inhibited the infiltration of mononuclear cells and reduced CC chemokine content in the peritoneal exudate. Pretreatment with either an anti-TNFα or an anti-IL-4 antiserum decreased Ang-II-induced arteriolar mononuclea…

MaleUmbilical Veinsmedicine.medical_specialtyEndotheliummedicine.medical_treatmentImmunologyBiologyBiochemistryPeripheral blood mononuclear cellMicrocirculationRats Sprague-DawleyInternal medicineCell AdhesionmedicineAnimalsHumansVasoconstrictor AgentsRNA MessengerVenuleReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaAngiotensin IICell BiologyHematologyAngiotensin IIRatsArteriolesMononuclear cell infiltrationmedicine.anatomical_structureCytokineEndocrinologyLeukocytes MononuclearTumor necrosis factor alphaEndothelium VascularInterleukin-4ChemokinesInjections IntraperitonealBlood
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CXCR2 blockade impairs angiotensin II-induced CC chemokine synthesis and mononuclear leukocyte infiltration.

2007

Objective—Angiotensin II (Ang-II) and mononuclear leukocytes are involved in atherosclerosis. This study reports the inhibition of Ang-II–induced mononuclear cell recruitment by CXCR2 antagonism and the mechanisms involved.Methods and Results—Ang-II (1 nmol/L, i.p. in rats) induced CXC and CC chemokines, followed by neutrophil and mononuclear cell recruitment. Administration of the CXCR2 antagonist, SB-517785-M, inhibited the infiltration of both neutrophils (98%) and mononuclear cells (60%). SB-517785-M had no effect on the increase in CXC chemokine levels but reduced MCP-1, RANTES, and MIP-1α release by 66%, 63%, and 80%, respectively. Intravital microscopy showed that pretreatment with S…

Malemedicine.medical_specialtyChemokineCXCR3Peripheral blood mononuclear cellLosartanReceptors Interleukin-8BRats Sprague-DawleyChemokine receptorInternal medicinemedicineCell AdhesionCCL17AnimalsHumansCXC chemokine receptorsSplanchnic CirculationChemokine CCL7Chemokine CCL4Chemokine CCL5Cells CulturedChemokine CCL2Chemokine CCL3InflammationbiologyAngiotensin IIMicrocirculationEndothelial CellsMacrophage Inflammatory ProteinsAtherosclerosisAngiotensin IIMonocyte Chemoattractant ProteinsRatsMononuclear cell infiltrationChemotaxis LeukocyteEndocrinologyNeutrophil Infiltrationbiology.proteinLeukocytes MononuclearCardiology and Cardiovascular MedicineAngiotensin II Type 1 Receptor BlockersArteriosclerosis, thrombosis, and vascular biology
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Angiotensin II Induces Neutrophil Accumulation In Vivo Through Generation and Release of CXC Chemokines

2004

Background—Angiotensin II (Ang II) is implicated in the development of cardiac ischemic disorders in which prominent neutrophil accumulation occurs. Ang II can be generated intravascularly by the renin-angiotensin system or extravascularly by mast cell chymase. In this study, we characterized the ability of Ang II to induce neutrophil accumulation.Methods and Results—Intraperitoneal administration of Ang II (1 nmol/L) induced significant neutrophil recruitment within 4 hours (13.3±2.3×106neutrophils per rat versus 0.7±0.5×106in control animals), which disappeared by 24 hours. Maximal levels of CXC chemokines were detected 1 hour after Ang II injection (577±224 pmol/L cytokine-inducible neut…

MaleChemokinemedicine.medical_specialtyEndotheliumCellsInflammationAngiotensin ; Interleukins ; Cells ; Endothelium ; InflammationPulmonary ArteryUmbilical CordRats Sprague-DawleyAngiotensin:CIENCIAS MÉDICAS ::Medicina interna [UNESCO]Physiology (medical)Internal medicineRenin–angiotensin systemCell AdhesionLeukocytesAnimalsHumansMedicineMesenteryRNA MessengerEndotheliumPeritoneal CavityMacrophage inflammatory proteinCells CulturedUNESCO::CIENCIAS MÉDICAS ::Medicina internaInflammationbiologybusiness.industryAngiotensin IIMicrocirculationInterleukinsInterleukin-8Endothelial CellsChemotaxis:CIENCIAS MÉDICAS [UNESCO]Angiotensin IIRatsmedicine.anatomical_structureEndocrinologyNeutrophil InfiltrationUNESCO::CIENCIAS MÉDICASbiology.proteinmedicine.symptomCardiology and Cardiovascular MedicinebusinessChemokines CXCIntravital microscopy
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Angiotensin II-Induced Mononuclear Leukocyte Interactions with Arteriolar and Venular Endothelium Are Mediated by the Release of Different CC Chemoki…

2006

Abstract Angiotensin II (Ang-II) is associated with atherogenesis and arterial subendothelial mononuclear leukocyte infiltration. We have demonstrated that Ang-II causes the initial attachment of mononuclear cells to the arteriolar endothelium. We now report on the contribution of CC chemokines to this response. Intraperitoneal administration of 1 nM Ang-II induced MCP-1, RANTES, and MIP-1α generation, maximal at 4 h, followed by mononuclear leukocyte recruitment at 8 and 24 h. Using intravital microscopy within the rat mesenteric microcirculation 4 h after exposure to 1 nM Ang-II, arteriolar mononuclear cell adhesion was 80–90% inhibited by pretreatment with Met-RANTES, a CCR1 and CCR5 ant…

MaleCCR1EndotheliumImmunologyVascular Cell Adhesion Molecule-1Peripheral blood mononuclear cellUmbilical CordRats Sprague-DawleyLeukocyte CountCell MovementCell AdhesionLeukocytesmedicineAnimalsHumansImmunology and AllergyEndotheliumChemokine CCL5Cells CulturedChemokine CCL2Angiotensin II receptor type 1Chemokine CCL26business.industryAngiotensin IIMonocyteEpithelial Cellsmedicine.diseaseAngiotensin IIMolecular biologyRatsP-Selectinmedicine.anatomical_structureChemokines CCImmunologycardiovascular systembusinessInfiltration (medical)Intravital microscopyThe Journal of Immunology
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L-NAME induces direct arteriolar leukocyte adhesion, which is mainly mediated by angiotensin-II.

2005

Acute inhibition (1 h) of nitric oxide synthase (NOS) with L-NAME causes leukocyte recruitment in the rat mesenteric postcapillary venules that is angiotensin-II (Ang-II) dependent. Since 4-h exposure to Ang-II provokes arteriolar leukocyte adhesion, this study was designed to investigate whether subacute (4-h) NOS inhibition also causes this effect.Rats were intraperitoneally injected with saline, L-NAME, or 1H-[1,2,4]-oxidazolol-[4,3-a]-quinoxalin-1-one (ODQ). Leukocyte accumulation in the mesenteric microcirculation was examined 4 h later via intravital microscopy. Some groups were pretreated with losartan, an AT(1) Ang-II receptor antagonist.At 4-h, L-NAME caused a significant increase …

MaleEndotheliumPhysiologyPharmacologyLosartanNitric oxideRats Sprague-Dawleychemistry.chemical_compoundVenulesPhysiology (medical)medicineCell AdhesionLeukocytesAnimalsLeukocyte RollingSplanchnic CirculationReceptorMolecular BiologyAngiotensin II receptor type 1Microscopy VideobiologyAngiotensin IIAngiotensin IIRatsNitric oxide synthaseArteriolesmedicine.anatomical_structureLosartanNG-Nitroarginine Methyl EsterchemistryImmunologycardiovascular systembiology.proteinNitric Oxide SynthaseCardiology and Cardiovascular MedicineCell Adhesion MoleculesIntravital microscopymedicine.drugMicrocirculation (New York, N.Y. : 1994)
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Erythromycin exertsin vivoanti-inflammatory activity downregulating cell adhesion molecule expression

2005

1. Macrolides have long been used as anti-bacterial agents; however, there is some evidence that may exert anti-inflammatory activity. Therefore, erythromycin was used to characterize the mechanisms involved in their in vivo anti-inflammatory activity. 2. Erythromycin pretreatment (30 mg kg(-1) day(-1) for 1 week) reduced the lipopolysaccharide (LPS; intratracheal, 0.4 mg kg(-1))-induced increase in neutrophil count and elastase activity in the bronchoalveolar lavage fluid (BALF) and lung tissue myeloperoxidase activity, but failed to decrease tumor necrosis factor-alpha and macrophage-inflammatory protein-2 augmented levels in BALF. Erythromycin pretreatment also prevented lung P-selectin,…

Pharmacologymedicine.diagnostic_testLipopolysaccharideCell adhesion moleculeErythromycinPharmacologyBiologychemistry.chemical_compoundBronchoalveolar lavagechemistryIn vivoImmunologymedicineTumor necrosis factor alphaCell adhesionmedicine.drugAntibacterial agentBritish Journal of Pharmacology
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Disruption of the CCL1-CCR8 axis inhibits vascular Treg recruitment and function and promotes atherosclerosis in mice

2019

The CC chemokine 1 (CCL1, also called I-309 or TCA3) is a potent chemoattractant for leukocytes that plays an important role in inflammatory processes and diseases through binding to its receptor CCR8. Here, we investigated the role of the CCL1-CCR8 axis in atherosclerosis. We found increased expression of CCL1 in the aortas of atherosclerosis-prone fat-fed apolipoprotein E (Apoe)-null mice; moreover, in vitro flow chamber assays and in vivo intravital microscopy demonstrated an essential role for CCL1 in leukocyte recruitment. Mice doubly deficient for CCL1 and Apoe exhibited enhanced atherosclerosis in aorta, which was associated with reduced plasma levels of the anti-inflammatory interle…

0301 basic medicineApolipoprotein Emedicine.medical_specialtyRegulatory T cellCCL1030204 cardiovascular system & hematologyCCR8T-Lymphocytes RegulatoryReceptors CCR8Chemokine CCL1Mice03 medical and health sciencesApolipoproteins ETh2 Cells0302 clinical medicineInternal medicineLeukocytesmedicineSplenocyteAnimalsMolecular BiologyInflammationMice KnockoutChemistryTh1 CellsAtherosclerosisInterleukin-10Mice Inbred C57BLTregInterleukin 10030104 developmental biologyEndocrinologymedicine.anatomical_structureIL-10CytokinesCardiology and Cardiovascular MedicineCCR8Intravital microscopyCCL1LipoproteinJournal of Molecular and Cellular Cardiology
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Contributions of ACE and mast cell chymase to endogenous angiotensin II generation and leucocyte recruitment in vivo

2011

Aims In vitro studies suggest that mast cell chymase (MCP) is more important than angiotensin-converting enzyme (ACE) for generating angiotensin II (Ang II) within the cardiovascular system. We investigated in vivo the relative contributions of ACE and MCP to leucocyte recruitment induced by endogenously generated Ang II. Methods and results Exposure of the murine cremasteric microcirculation of C57BL/6 mice to Ang I (100 nM for 4 h) induced leucocyte–endothelium interactions. Either losartan (an Ang II receptor-1 antagonist, AT1) or enalapril (an ACE inhibitor), but not chymostatin (a chymase inhibitor), inhibited Ang I-induced responses. Mast cell degranulation with compound 48/80 (CMP48/…

Malemedicine.medical_specialtyPhysiologymedicine.drug_classReceptor expressionPeptidyl-Dipeptidase AReceptor Angiotensin Type 1MiceChymasesCell MovementPhysiology (medical)Internal medicineLeukocytesmedicineAnimalsp-Methoxy-N-methylphenethylamineMast CellsMast cell stabilizerEnalaprilAngiotensin II receptor type 1ChemistryAngiotensin IIChymaseAngiotensin IIMice Inbred C57BLEndocrinologyLosartanACE inhibitorcardiovascular systemAngiotensin ICardiology and Cardiovascular Medicinehormones hormone substitutes and hormone antagonistsmedicine.drugCardiovascular Research
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Effect of boldine, secoboldine, and boldine methine on angiotensin II-induced neutrophil recruitment in vivo.

2005

AbstractAngiotensin-II (Ang-II) has inflammatory activity and is involved in different diseases associated with the cardiovascular system. This study has evaluated the effect of boldine (B), and two phenanthrene alkaloids semisynthesized by us, secoboldine (SB) and boldine methine (BM), on Ang-II-induced neutrophil recruitment. Intraperitoneal administration of 1 nM Ang-II induced significant neutrophil accumulation, which was maximal at 4–8 h. BM inhibited neutrophil infiltration into the peritoneal cavity at 4 h and 8 h by 73% and 77%, respectively, SB at 8 h by 55%, and B had no effect on this response. Although BM inhibited the release of cytokine-inducible neutrophil chemoattractant/ke…

KeratinocytesMaleChemokineAporphinesEndotheliumNeutrophilsImmunologyChemokine CXCL2InflammationPharmacologyRats Sprague-Dawleychemistry.chemical_compoundIn vivomedicineImmunology and AllergyBoldineAnimalsHumansInfusions ParenteralPlatelet Activating FactorReceptorchemistry.chemical_classificationReactive oxygen speciesbiologyMolecular StructureAngiotensin IIMonokinesInterleukin-8Endothelial CellsCell BiologyPhenanthrenesAngiotensin IIRatsP-Selectinmedicine.anatomical_structureBiochemistrychemistrybiology.proteinIntercellular Signaling Peptides and Proteinsmedicine.symptomChemokinesReactive Oxygen SpeciesChemokines CXCJournal of leukocyte biology
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A small molecule, orally active, α 4 β 1 /α 4 β 7 dual antagonist reduces leukocyte infiltration and airway hyper-responsiveness in an experimental m…

2006

α4β1 and α4β7 integrins are preferentially expressed on eosinophils and mononuclear leukocytes and play critical roles in their recruitment to inflammatory sites. We investigated the effects of TR14035, a small molecule, α4β1/α4β7 dual antagonist, in a rat model of allergic asthma. Actively sensitized rats were challenged with aerosol antigen or saline on day 21, and the responses evaluated 24 and 48-h later. TR14035 (3 mg kg−1, p.o.) was given 1-h before and 4-h after antigen or saline challenge. Airway hyper-responsiveness to intravenous 5-hydroxytryptamine was suppressed in TR14035-treated rats. Eosinophil, mononuclear cell and neutrophil counts, and eosinophil peroxidase and protein con…

Pharmacologymedicine.diagnostic_testbiologybusiness.industryInterleukinEosinophilPeripheral blood mononuclear cellBronchoalveolar lavagemedicine.anatomical_structureImmunologymedicinebiology.proteinCell adhesionbusinessEosinophil peroxidaseInterleukin 5Intravital microscopyBritish Journal of Pharmacology
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Direct evidence of leukocyte adhesion in arterioles by angiotensin II

2004

AbstractAlthough leukocytes adhere in arteries in various vascular diseases, to date no endogenous proinflammatory molecule has been identified to initiate leukocyte adhesion in the arterial vasculature. This study was undertaken to assess angiotensin II (Ang II)-induced leukocyte adhesion in arterioles in vivo. Rats received intraperitoneal injections of Ang II; 4 hours later, leukocyte recruitment in mesenteric microcirculation was examined using intravital microscopy. Ang II (1 nM) produced significant arteriolar leukocyte adhesion of mononuclear cells. Using function-blocking monoclonal antibodies (mAbs) against different rat cell adhesion molecules (CAMs), we discovered that this effec…

Malemedicine.medical_specialtyEndotheliumIntegrin alpha4ImmunologyIntercellular Adhesion Molecule-1Vascular Cell Adhesion Molecule-1BiologyBiochemistryRats Sprague-DawleyVenulesInternal medicineCell AdhesionLeukocytesmedicineAnimalsVasoconstrictor AgentsLeukocyte RollingCell adhesionCell adhesion moleculeAngiotensin IINF-kappa BCell BiologyHematologyIntercellular Adhesion Molecule-1Angiotensin IIRatsArteriolesmedicine.anatomical_structureEndocrinologyCD18 AntigensImmunologyEndothelium VascularIntravital microscopySelectinArteryBlood
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