Isabella Fiorentino

University of Naples Federico II

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Nella Prevete

University of Naples Federico II

Amato de Paulis

University of Naples Federico II

Gianni Marone

University of Naples Federico II

Valeria Angri

University of Naples Federico II

Plinio Cirillo

University of Naples Federico II

Mario Pacileo

Policlinico Umberto I

Salvatore De Rosa

Magna Graecia University

Grazia Ucci

University of Naples Federico II

Massimo Chiariello

University of Naples Federico II

Laura Sasso

Azienda Ospedaliero-Universitaria Careggi

Cooperative Institutions

University of Naples Federico II

Federico II University Hospital

National Research Council

Inserm

University of Campania "Luigi Vanvitelli"

Istituti di Ricovero e Cura a Carattere Scientifico

Ludwig-Maximilians-Universität München

University of Salerno

Institute for Experimental Endocrinology and Oncology

National Institutes of Health

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Neopterin induces pro‐atherothrombotic phenotype in human coronary endothelial cells

Journal of Thrombosis and Haemostasis (2006)

Plinio Cirillo Mario Pacileo Salvatore De Rosa Paolo Calabrò Annarita Gargiulo

Neopterin

10.1111/j.1538-7836.2006.02125.x

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Citations (47)

Author Index Vol. 44, 2007

Journal of Vascular Research (2007)

Zhaoqing Yang Dmitry Gagarin Ali Ramezani Awahan Rahman Louise Holm Schæbel

10.1159/000110047

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Basophils Infiltrate Human Gastric Mucosa at Sites of Helicobacter pylori Infection, and Exhibit Chemotaxis in Response to H. pylori-derived Peptide Hp(2–20)

The Journal of Immunology (2004)

Amato de Paulis Nella Prevete Isabella Fiorentino Andrew F. Walls Monica Curto

Abstract Basophils, which are normally confined to the circulation, can migrate to sites of allergic inflammation. Using the specific mAb, BB1, we detected basophil infiltration of the gastric mucosa of Helicobacter pylori-infected patients affected by moderate and severe gastritis. Basophils were not found in H. pylori-free individuals or in subjects with mild gastritis. The H. pylori-derived peptide, Hp(2–20), was a potent basophil chemoattractant in vitro, whereas the control peptide, Hp1, was ineffective. Basophils from peripheral blood of healthy volunteers expressed mRNA for the formyl peptide receptors, N-formyl-peptide receptor (FPR), FPR-like (FPRL)1, and FPRL2. Preincubation of basophils with FMLP or Hp(2–20) caused complete desensitization to a subsequent challenge with homologous stimulus. Incubation of basophils with a low concentration of FMLP, which binds with high affinity to FPR, but not to FPRL1 or FPRL2, did not affect the chemotactic response to Hp(2–20). In contrast, a high concentration of FMLP, which binds to FPRL1 and FPRL2, reduced the chemotactic response to Hp(2–20). The FPR antagonist, cyclosporin H, prevented chemotaxis induced by FMLP, but not by Hp(2–20). Hp(2–20) could be responsible, at least in part, for basophil infiltration of the gastric mucosa of H. pylori-infected patients presumably through the interaction with FPRL1 and FPRL2.

Formyl peptide receptor

Infiltration (HVAC)

Interleukin 8

10.4049/jimmunol.172.12.7734

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Citations (68)

Erratum

Journal of Vascular Research (2007)

Zhaoqing Yang Dmitry Gagarin A Ramezani Awahan Rahman Louise Holm Schæbel

10.1159/000110050

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HIV-1 Envelope gp41 Peptides Promote Migration of Human FcεRI+ Cells and Inhibit IL-13 Synthesis Through Interaction with Formyl Peptide Receptors

The Journal of Immunology (2002)

Amato de Paulis Giovanni Florio Nella Prevete Massimo Triggiani Isabella Fiorentino

Abstract We evaluated the effects of synthetic peptides (2017, 2019, 2020, 2021, 2023, 2027, 2029, 2030, 2031, and 2035) encompassing the structure of HIV-1MN envelope gp41 on both chemotaxis of human basophils and the release of preformed mediators (histamine) and of cytokines (IL-13). Peptides 2019 and 2021 were potent basophil chemoattractants, whereas the other peptides examined were ineffective. Preincubation of basophils with FMLP or gp41 2019 resulted in complete desensitization to a subsequent challenge with homologous stimulus. Incubation of basophils with low concentration (5 × 10−7 M) of FMLP, which binds with high affinity to N-formyl peptide receptor (FPR), but not to FPR-like 1, did not affect the chemotactic response to a heterologous stimulus (gp41 2019). In contrast, a high concentration (10−4 M) of FMLP, which binds also to FPR-like 1, significantly reduced the chemotactic response to gp41 2019. The FPR antagonist cyclosporin H inhibited chemotaxis induced by FMLP, but not by gp41 2019. None of these peptides singly induced the release of histamine or cytokines (IL-4 and IL-13) from basophils. However, low concentrations of peptides 2019 and 2021 (10−8–10−6 M) inhibited histamine release from basophils challenged with FMLP but not the secretion caused by anti-IgE and gp120. Preincubation of basophils with peptides 2019 and 2021 inhibited the expression of both IL-13 mRNA, and the FMLP-induced release of IL-13 from basophils. These data highlight the complexity of the interactions between viral and bacterial peptides with FPR subtypes on human basophils.

Homologous desensitization

Formyl peptide receptor

N-Formylmethionine leucyl-phenylalanine

10.4049/jimmunol.169.8.4559

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Citations (34)

Activation of human basophils and mast cells by superallergens. The Batsheva de Rothschild International Workshop on Mast Cell Signalling and Function in Health and Disease

Gianni Marone Nella Prevete Gianluca De Rienzo Isabella Fiorentino Francesca Wanda Rossi

Mast (botany)

Rothschild

Interleukin 33

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Urokinase Induces Basophil Chemotaxis through a Urokinase Receptor Epitope That Is an Endogenous Ligand for Formyl Peptide Receptor-Like 1 and -Like 2

The Journal of Immunology (2004)

Amato de Paulis Nunzia Montuori Nella Prevete Isabella Fiorentino Francesca Wanda Rossi

Abstract Basophils circulate in the blood and are able to migrate into tissues at sites of inflammation. Urokinase plasminogen activator (uPA) binds a specific high affinity surface receptor (uPAR). The uPA-uPAR system is crucial for cell adhesion and migration, and tissue repair. We have investigated the presence and function of the uPA-uPAR system in human basophils. The expression of uPAR was found at both mRNA and protein levels. The receptor was expressed on the cell surface of basophils, in the intact and cleaved forms. Basophils did not express uPA at either the protein or mRNA level. uPA (10−12–10−9 M) and its uPAR-binding N-terminal fragment (ATF) were potent chemoattractants for basophils, but did not induce histamine or cytokine release. Inactivation of uPA enzymatic activity by di-isopropyl fluorophosphate did not affect its chemotactic activity. A polyclonal Ab against uPAR inhibited uPA-dependent basophil chemotaxis. The uPAR-derived peptide 84–95 (uPAR84–95) induced basophil chemotaxis. Basophils expressed mRNA for the formyl peptide receptors formyl peptide receptor (FPR), FPR-like 1 (FPRL1), and FPRL2. The FPR antagonist cyclosporin H prevented chemotaxis induced by FMLP, but not that induced by uPA and uPAR84–95. Incubation of basophils with low and high concentrations of FMLP, which desensitize FPR and FPRL1, respectively, but not FPRL2, slightly reduced the chemotactic response to uPA and uPAR84–95. In contrast, desensitization with WKYMVm, which also binds FPRL2, markedly inhibited the response to both molecules. Thus, uPA is a potent chemoattractant for basophils that seems to act through exposure of the chemotactic uPAR epitope uPAR84–95, which is an endogenous ligand for FPRL2 and FPRL1.

10.4049/jimmunol.173.9.5739

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HMG-CoA Reductase Inhibitors Reduce Nicotine-Induced Expression of Cellular Adhesion Molecules in Cultured Human Coronary Endothelial Cells

Journal of Vascular Research (2007)

Plinio Cirillo Mario Pacileo Salvatore De Rosa Paolo Calabrò Annarita Gargiulo

Smoking predisposes to the development of atherosclerosis and of its complications. The mechanisms responsible for these effects are not completely understood. We have investigated whether nicotine might promote a proatherosclerotic state in human coronary endothelial cells (HCAECs), studying the role of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors in preventing these phenomena.Real-time PCR showed that nicotine induced a dose-dependent increase in mRNA levels for vascular cellular adhesion molecule-1 (VCAM-1)/intercellular adhesion molecule-1 (ICAM-1). Fluorescent-activated cell sorting analysis showed that nicotine induced expression of functionally active VCAM-1/ICAM-1, since they increased leukocyte adherence to HCAECs. Oxygen free radicals, Rho A and nuclear factor kappaB (NF-kappaB) play a pivotal role in modulating these effects. Indeed, nicotine caused oxygen free radical production as well as activation of Rho A and NF-kappaB pathways, evaluated by malondialdehyde levels, pulldown assay and by electrophoretic mobility shift assay, respectively. Superoxide dimutase, Rho A (Y-27639) and NF-kappaB inhibitors (pyrrolidine dithiocarbamate ammonium, Bay 11-7082) suppressed nicotine effects on CAM expression. HMG-CoA reductase inhibitors prevented these nicotine-mediated effects by inhibiting free radical generation and by modulating activation of Rho A and NF-kappaB pathways.Nicotine promotes CAM expression on HCAECs, shifting them toward a proatherosclerotic state. These effects might explain, at least in part, the deleterious cardiovascular consequences of cigarette smoking. HMG-CoA reductase inhibitors play an important role in preventing these phenomena.

10.1159/000106464

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Citations (27)

Roles of mast cells and their mediators in human thyroid carcinomas

Hormone Research in Paediatrics (2007)

Rm Melillo Amato de Paulis Guarino Galdiero Nella Prevete

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Expression and Functions of the Vascular Endothelial Growth Factors and Their Receptors in Human Basophils

The Journal of Immunology (2006)

Amato de Paulis Nella Prevete Isabella Fiorentino Francesca Wanda Rossi Stefania Staibano

Abstract Angiogenesis is a multistep complex phenomenon critical for several inflammatory and neoplastic disorders. Basophils, normally confined to peripheral blood, can infiltrate the sites of chronic inflammation. In an attempt to obtain insights into the mechanism(s) underlying human basophil chemotaxis and its role in inflammation, we have characterized the expression and function of vascular endothelial growth factors (VEGFs) and their receptors in these cells. Basophils express mRNA for three isoforms of VEGF-A (121, 165, and 189) and two isoforms of VEGF-B (167 and 186). Peripheral blood and basophils in nasal polyps contain VEGF-A localized in secretory granules. The concentration of VEGF-A in basophils was 144.4 ± 10.8 pg/106 cells. Immunologic activation of basophils induced the release of VEGF-A. VEGF-A (10–500 ng/ml) induced basophil chemotaxis. Supernatants of activated basophils induced an angiogenic response in the chick embryo chorioallantoic membrane that was inhibited by an anti-VEGF-A Ab. The tyrosine kinase VEGFR-2 (VEGFR-2/KDR) mRNA was expressed in basophils. These cells also expressed mRNA for the soluble form of VEGFR-1 and neuropilin (NRP)1 and NRP2. Flow cytometric analysis indicated that basophils express epitopes recognized by mAbs against the extracellular domains of VEGFR-2, NRP1, and NRP2. Our data suggest that basophils could play a role in angiogenesis and inflammation through the expression of several forms of VEGF and their receptors.

Allergic Inflammation

10.4049/jimmunol.177.10.7322

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Citations (125)