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Blood, 15 September 2007, Vol. 110, No. 6, pp. 1895-1902.
Prepublished online as a Blood First Edition Paper on June 26, 2007; DOI 10.1182/blood-2007-01-070607.
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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
A critical role for TNF in the selective attachment of mononuclear leukocytes to angiotensin-II-stimulated arterioles
Teresa Mateo1,
Yafa Naim Abu Nabah1,
Mercedes Losada1,
Rossana Estellés1,
Chantal Company1,
Begoña Bedrina1,
Jose Miguel Cerdá-Nicolás2,3,
Stephen Poole4,
Peter J. Jose1,
Julio Cortijo1,3,5,
Esteban J. Morcillo1,3,6, and
Maria-Jesus Sanz1,3
1 Department of Pharmacology and
2 Department of Pathology, Faculty of Medicine, University of Valencia, Spain;
3 Ciber CB06/06/0027 "Respiratory Diseases" Carlos III Health Institute, Spanish Ministry of Health, Madrid, Spain;
4 Division of Endocrinology, National Institute for Biological Standards and Control, Potters Bar, United Kingdom;
5 Research Foundation, University General Hospital Consortium, Valencia, Spain; and
6 Clinical Pharmacology Unit, University Clinical Hospital, Valencia, Spain
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 (TNF ) in the leukocyte accumulation elicited by Ang-II. Ang-II (1 nM intraperitoneally in rats) induced TNF release at 1 hour followed by neutrophil and mononuclear cell recruitment. The administration of an antirat TNF 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-TNF or an anti-IL-4 antiserum decreased Ang-II-induced arteriolar mononuclear leukocyte adhesion by 68% and 60%, respectively, in the rat mesenteric microcirculation. While no expression of TNF was found in the postcapillary venules of Ang-II-injected animals, this cytokine was clearly up-regulated in the arterioles. Stimulation of human umbilical arterial endothelial cells (HUAECs) or isolated human mononuclear cells with 1 µM Ang-II caused increased TNF mRNA expression and protein. Neutralization of TNF activity reduced Ang-II-induced MCP-1, MCP-3, and RANTES release from HUAECs and MIP-1 from blood cells. In conclusion, the selective mononuclear leukocyte adhesion to Ang-II-stimulated arterioles is largely mediated by TNF in cooperation with constitutive IL-4. Therefore, neutralization of TNF activity may help to prevent mononuclear cell infiltration and the progression of the atherogenic process.
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