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Methylenedioxymethamphetamine (Ecstasy) Decreases Neutrophil Activity and Alters Leukocyte Distribution in Bone Marrow, Spleen and Blood

PAULA, Viviane Ferraz de; RIBEIRO, Alison; PINHEIRO, Milena L.; SAKAI, Monica; LACAVA, Mariana C. R.; LAPACHINSKE, Silvio F.; MOREAU, Regina L. M.; PALERMO-NETO, Joao
Fonte: KARGER Publicador: KARGER
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
36.81%
Objective: Looking for possible neuroimmune relationships, we analyzed the effects of methylenedioxymethamphetamine (MDMA) administration on neuroendocrine, neutrophil activity and leukocyte distribution in mice. Methods: Five experiments were performed. In the first, mice were treated with MDMA (10 mg/kg) 30, 60 min and 24 h prior to blood sample collection for neutrophil activity analysis. In the second experiment, the blood of nave mice was collected and incubated with MDMA for neutrophil activity in vitro analysis. In the third and fourth experiments, mice were injected with MDMA (10 mg/kg) and 60 min later, blood and brain were collected to analyze corticosterone serum levels and hypothalamic noradrenaline (NA) levels and turnover. In the last experiment, mice were injected with MDMA 10 mg/kg and 60 min later, blood, bone marrow and spleen were collected for leukocyte distribution analysis. Results: Results showed an increase in hypothalamic NA turnover and corticosterone serum levels 60 min after MDMA (10 mg/kg) administration, a decrease in peripheral blood neutrophil oxidative burst and a decrease in the percentage and intensity of neutrophil phagocytosis. It was further found that MDMA (10 mg/kg) treatment also altered leukocyte distribution in blood...

Effects of chlorogenic acid on neutrophil locomotion functions in response to inflammatory stimulus

HEBEDA, C. B.; BOLONHEIS, S. M.; NAKASATO, A.; BELINATI, K.; SOUZA, P. D. C.; GOUVEA, D. R.; LOPES, N. P.; FARSKY, S. H. P.
Fonte: ELSEVIER IRELAND LTD Publicador: ELSEVIER IRELAND LTD
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
36.75%
Aim of the study: Species of Lychnophora are used in Brazilian folk medicine as analgesic and anti-inflammatory agents. Chlorogenic acid (CGA) and their analogues are important components of polar extracts of these species, as well in several European and Asian medicinal plants. Some of these phenolic compounds display anti-inflammatory effects. In this paper we report the isolation of CGA from Lychnophora salicifolia and its effects on functions involved in neutrophils locomotion. Materials and methods: LC-MS(n) data confirmed the presence of CGA in the plant. Actions of CGA were investigated on neutrophils obtained from peritoneal cavity of Wistar rats (4h after 1% oyster glycogen solution injection; 10 ml), and incubated with vehicle or with 50, 100 or 1000 mu M CGA in presence of lipopolysaccharide from Escherichia coil (LPS, 5 mu g/ml). Nitric oxide (NO; Griess reaction); prostaglandin E(2) (PGE(2)), interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha [TNF-alpha; enzyme-linked immunosorbent assay (EIA)]; protein (flow cytometry) and gene (RT-PCR) expression of L-selectin, beta(2)integrin and platelet-endothelial cell adhesion molecule-1 (PECAM-1) were quantified. In vitro neutrophil adhesion to primary culture of microvascular endothelial cell (PMEC) and neutrophil migration in response to formyl-methionil-leucil-phenilalanine (fMLP...

Neutrophil migration induced by IL-1 beta depends upon LTB4 released by macrophages and upon TNF-alpha and IL-1 beta released by mast cells

OLIVEIRA, S. H. P.; CANETTI, C.; RIBEIRO, R. A.; CUNHA, F. Q.
Fonte: SPRINGER/PLENUM PUBLISHERS Publicador: SPRINGER/PLENUM PUBLISHERS
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
36.81%
In the present study, we investigate whether mast cells and macrophages are involved in the control of IL-1 beta-induced neutrophil migration, as well as the participation of chemotactic mediators. IL-1 beta induced a dose-dependent neutrophil migration to the peritoneal cavity of rats which depends on LTB4, PAF and cytokines, since the animal treatment with inhibitors of these mediators (MK 886, PCA 4248 and dexamethasone respectively) inhibited IL-1 beta-induced neutrophil migration. The neutrophil migration induced by IL-1 beta is dependent on mast cells and macrophages, since depletion of mast cells reduced the process whereas the increase of macrophage population enhanced the migration. Moreover, mast cells or macrophages stimulated with IL-1 beta released a neutrophil chemotactic factor, which mimicked the neutrophil migration induced by IL-1 beta. The chemotactic activity of the supernatant of IL-1 beta-stimulated macrophages is due to the presence of LTB4, since MK 886 inhibited its release. Moreover, the chemotactic activity of IL-1 beta-stimulated mast cells supernatant is due to the presence of IL-1 beta and TNF-alpha, since antibodies against these cytokines inhibited its activity. Furthermore, significant amounts of these cytokines were detected in the supernatant. In conclusion...

Inhibition of Neutrophil Migration by Hemopexin Leads to Increased Mortality Due to Sepsis in Mice

SPILLER, Fernando; COSTA, Carlotta; SOUTO, Fabricio O.; VINCHI, Francesca; MESTRINER, Fabiola L. A. C.; LAURE, Helen J.; ALVES-FILHO, Jose C.; FREITAS, Andressa; ROSA, Jose C.; FERREIRA, Sergio H.; ALTRUDA, Fiorella; HIRSCH, Emilio; GREENE, Lewis J.; TOLO
Fonte: AMER THORACIC SOC Publicador: AMER THORACIC SOC
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
36.89%
Rationale: The reduction of neutrophil migration to the bacterial focus is associated with poor outcome in sepsis. Objectives: The objective of this study was to identify soluble substances in the blood of septic mice that inhibit neutrophil migration. Methods: A pool of serum obtained from mice 2 hours after the induction of severe sepsis by cecal ligation and puncture inhibited the neutrophil migration. The proteins with inhibitory activity on neutrophil migration were isolated by Blue-Sepharose chromatography, high-performance liquid chromatography, and electrophoresis, and identified by mass spectrometry. Measurements and Main Results: Hemopexin was identified as the serum component responsible for the inhibition of neutrophil migration. In sepsis, the pretreatment of wild-type mice with hemopexin inhibited neutrophil migration to the focus of infection and decreased the survival rate from 87.5 to 50.0%. Hemopexin-null mice subjected to severe sepsis presented normal neutrophil migration, low bacteremia, and an improvement of 40% in survival rate. Moreover, hemopexin inhibited the neutrophil chemotaxis response evoked by C5a or macrophage inflammatory protein-2 and induced a reduction of CXCR2 and L-selectin as well as the up-regulation of CD11b expression in neutrophil membranes. The inhibitory effect of hemopexin on neutrophil chemotaxis was prevented by serine protease inhibitors or ATP. In addition...

Hydrogen Sulfide Improves Neutrophil Migration and Survival in Sepsis via K(ATP)(+) Channel Activation

SPILLER, Fernando; ORRICO, Maria I. L.; NASCIMENTO, Daniele C.; CZAIKOSKI, Paula G.; SOUTO, Fabricio O.; ALVES-FILHO, Jose C.; FREITAS, Andressa; CARLOS, Daniela; MONTENEGRO, Marcelo F.; Federman Neto, Alberto; FERREIRA, Sergio H.; ROSSI, Marcos A.; HOTHE
Fonte: AMER THORACIC SOC Publicador: AMER THORACIC SOC
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
36.79%
Rationale Recovering the neutrophil migration to the infectious focus improves survival in severe sepsis. Recently, we demonstrated that the cystathionine gamma-lyase (CSE)/hydrogen sulfide (H(2)S) pathway increased neutrophil recruitment to inflammatory focus during sterile inflammation. Objectives: To evaluate if H(2)S administration increases neutrophil migration to infectious focus and survival of mice. Methods. Sepsis was induced by cecal ligation and puncture (CLP) Measurements and Main Results. The pretreatments of mice with H2S donors (NaHS or Lawesson`s reagent) improved leukocyte rolling/adhesion in the mesenteric microcirculation as well as neutrophil migration. Consequently, bacteremia levels were reduced, hypotension and lung lesions were prevented, and the survival rate increased from approximately 13% to approximately 80% Even when treatment was delayed (6 h after CLP), a highly significant reduction in mortality compared with untreated mice was observed Moreover, H(2)S pretreatment prevented the down-regulation of CXCR2 and L-selectin and the up-regulation of CD11b and G protein-coupled receptor kinase 2 in neutrophils during sepsis. H(2)S also prevented the reduction of intercellular adhesion molecule-1 expression in the endothelium of the mesenteric microcirculation in severe sepsis Confirming the critical role of H(2)S on sepsis outcome...

A crucial role for TNF-alpha in mediating neutrophil influx induced by endogenously generated or exogenous chemokines, KC/CXCL1 and LIX/CXCL5

VIEIRA, S. M.; LEMOS, H. P.; GRESPAN, R.; NAPIMOGA, M. H.; DAL-SECCO, D.; FREITAS, A.; CUNHA, T. M.; VERRI JR., W. A.; SOUZA-JUNIOR, D. A.; JAMUR, M. C.; FERNANDES, K. S.; OLIVER, C.; SILVA, J. S.; TEIXEIRA, M. M.; CUNHA, F. Q.
Fonte: WILEY-BLACKWELL PUBLISHING, INC Publicador: WILEY-BLACKWELL PUBLISHING, INC
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
36.83%
Background and purpose: Chemokines orchestrate neutrophil recruitment to inflammatory foci. In the present study, we evaluated the participation of three chemokines, KC/CXCL1, MIP-2/CXCL2 and LIX/CXCL5, which are ligands for chemokine receptor 2 (CXCR2), in mediating neutrophil recruitment in immune inflammation induced by antigen in immunized mice. Experimental approach: Neutrophil recruitment was assessed in immunized mice challenged with methylated bovine serum albumin, KC/CXCL1, LIX/CXCL5 or tumour necrosis factor (TNF)-alpha. Cytokine and chemokine levels were determined in peritoneal exudates and in supernatants of macrophages and mast cells by elisa. CXCR2 and intercellular adhesion molecule 1 (ICAM-1) expression was determined using immunohistochemistry and confocal microscopy. Key results: Antigen challenge induced dose- and time-dependent neutrophil recruitment and production of KC/CXCL1, LIX/CXCL5 and TNF-alpha, but not MIP-2/CXCL2, in peritoneal exudates. Neutrophil recruitment was inhibited by treatment with reparixin (CXCR1/2 antagonist), anti-KC/CXCL1, anti-LIX/CXCL5 or anti-TNF-alpha antibodies and in tumour necrosis factor receptor 1-deficient mice. Intraperitoneal injection of KC/CXCL1 and LIX/CXCL5 induced dose- and time-dependent neutrophil recruitment and TNF-alpha production...

Reduction of ICAM-1 expression by carbon monoxide via soluble guanylate cyclase activation accounts for modulation of neutrophil migration

DAL-SECCO, Daniela; FREITAS, Andressa; ABREU, Monica A.; GARLET, Thiago P.; ROSSI, Marcos A.; FERREIRA, Sergio H.; SILVA, Joao S.; ALVES-FILHO, Jose C.; CUNHA, Fernando Q.
Fonte: SPRINGER Publicador: SPRINGER
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
36.75%
Previously, it was demonstrated that the heme/heme oxygenase (HO)/carbon monoxide (CO) pathway inhibits neutrophil recruitment during the inflammatory response. Herein, we addressed whether the inhibitory effect of the HO pathway on neutrophil adhesion and migration involves the reduction of intracellular adhesion molecule type (ICAM)-1 and beta(2)-integrin expression. Mice pretreated with a specific inhibitor of inducible HO (HO-1), zinc protoporphyrin (ZnPP) IX, exhibit enhanced neutrophil adhesion and migration induced by intraperitoneal injection of Escherichia coli lipopolysaccharide (LPS). These findings are associated with an increase in ICAM-1 expression on mesentery venular endothelium. In accordance, HO-1 inhibition did not enhance LPS-induced neutrophil migration and adhesion in ICAM-1-deficient mice. Furthermore, the treatment with a CO donor (dimanganese decacarbonyl, DMDC) that inhibits adhesion and migration of the neutrophils, reduced LPS-induced ICAM-1 expression. Moreover, neither DMDC nor ZnPP IX treatments changed LPS-induced beta(2)-integrin expression on neutrophils. The effect of CO on ICAM-1 expression seems to be dependent on soluble guanylate cyclase (sGC) activation, since 1H-(1,2,4)oxadiazolo (4,3-a)quinoxalin-1-one (sGC inhibitor) prevented the observed CO effects. Finally...

Neutrophil activation induced by ArtinM: Release of inflammatory mediators and enhancement of effector functions

TOLEDO, Karina Alves; SCWARTZ, Carolina; OLIVEIRA, Aline Ferreira; CONRADO, Marina Cavalcanti Albuquerque Veiga; BERNARDES, Emerson Soares; FERNANDES, Luiz Claudio; ROQUE-BARREIRA, Maria Cristina; PEREIRA-DA-SILVA, Gabriela; MORENO, Andra Novais
Fonte: ELSEVIER SCIENCE BV Publicador: ELSEVIER SCIENCE BV
Tipo: Artigo de Revista Científica
Português
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36.75%
The D-mannose binding lectin ArtinM from Artocarpus integrifolia, previously known as KM+ and artocarpin. is considered a stimulant of Th1-type immunity, which is able to confer resistance to some intracellular pathogens. In addition, ArtinM induces neutrophil migration by haptotaxis through simultaneous interactions of its carbohydrate recognition domains (CRDs) with glycans expressed on the extracellular matrix and the neutrophil surface. In the present study, we have expanded the characterization of ArtinM as a neutrophil activator. Exposure of neutrophils to ArtinM for 15 min resulted in tyrosine phosphorylation of intracellular proteins, a process that was selectively inhibited by D-mannose or mannotriose. Shortly after stimulation, neutrophils secreted high levels of LTB(4) and underwent shedding of L-selectin from their surface. Exposure to ArtinM enhanced neutrophil functions, such as respiratory burst and zymozan and Listeria monocytogenes phagocytosis. In addition, ArtinM-stimulated neutrophils displayed increased CXCL-8 secretion and TLR2 gene transcription. These results demonstrate that ArtinM is able to induce potent neutrophil activation, a feature that should be strongly considered in the assessment of the lectin capacity to confer resistance against infections. (C) 2009 Elsevier B.V. All rights reserved.; FAPESP; CNPq; CAPES; FAEPA

Endothelin-1 induces neutrophil recruitment in adaptive inflammation via TNF alpha and CXCL1/CXCR2 in mice

Zarpelon, Ana C.; Pinto, Larissa G.; Cunha, Thiago M.; Vieira, Silvio M.; Carregaro, Vanessa; Souza, Guilherme R.; Silva, Joao S.; Ferreira, Sergio H.; Cunha, Fernando Q.; Verri, Waldiceu A., Jr.
Fonte: CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS; OTTAWA Publicador: CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS; OTTAWA
Tipo: Artigo de Revista Científica
Português
Relevância na Pesquisa
36.83%
Endothelin mediates neutrophil recruitment during innate inflammation. Herein we address whether endothelin-1 (ET-1) is involved in neutrophil recruitment in adaptive inflammation in mice, and its mechanisms. Pharmacological treatments were used to determine the role of endothelin in neutrophil recruitment to the peritoneal cavity of mice challenged with antigen (ovalbumin) or ET-1. Levels of ET-1, tumour necrosis factor a (TNF alpha), and CXC chemokine ligand 1 (CXCL1) were determined by enzyme-linked immunosorbent assay. Neutrophil migration and flow cytometry analyses were performed 4 h after the intraperitoneal stimulus. ET-1 induced dose-dependent neutrophil recruitment to the peritoneal cavity. Treatment with the non-selective ETA/ETB receptor antagonist bosentan, and selective ETA or ETB receptor antagonists BQ-123 or BQ-788, respectively, inhibited ET-1- and ovalbumin-induced neutrophil migration to the peritoneal cavity. In agreement with the above, the antigen challenge significantly increased levels of ET-1 in peritoneal exudates. The ET-1- and ovalbumin-induced neutrophil recruitment were reduced in TNFR1 deficient mice, and by treatments targeting CXCL1 or CXC chemokine receptor 2 (CXCR2); further, treatment with bosentan...

Efeitos de benzodiazepínicos sobre a atividade de neutrófilos de ratos avaliados por citometria de fluxo; Effects of benzodiazepines on rat neutrophil activity measured by flow cytometry

Silva, Fábio Ribeiro da
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Tese de Doutorado Formato: application/pdf
Publicado em 19/09/2003 Português
Relevância na Pesquisa
36.9%
Benzodiazepínicos (BDZ) são fármacos ansiolíticos que se caracterizam por atuar em receptores GABAa presentes no sistema nervoso central. Além dos receptores centrais os BDZ também possuem afinidade por sítios ligantes periféricos presentes em vários tecidos, dentre eles nas glândulas adrenais e em células polimorfonucleares. O presente experimento analisou os efeitos de BDZ sobre a atividade de neutrófilos e sobre os níveis séricos de corticosterona de ratos. Especificamente, o burst e a fagocitose de neutrófilos foram estudados após o tratamento ex vivo e in vitro com diazepam, RO 5-4864, clonazepam e/ou PK 11195. Os efeitos do diazepam sobre a atividade de neutrófilos também foram avaliados após o uso prolongado deste fármaco. Finalmente, os efeitos in vitro dos BDZ foram estudados após a incubação com um bloqueador do canal de cálcio (Ca2+) o L-verapamil. Os resultados mostraram que (1) o tratamento agudo ex vivo com diazepam (10 mg/kg) produziu um aumento do burst oxidativo e da fagocitose induzida por PMA, LPS e Staphylococcus aureus; (2) o tratamento prolongado (21 dias) com diazepam (10 mg/kg) produziu um aumento do burst oxidativo induzido pelos mesmos estímulos e reduziu a fagocitose dos neutrófilos (porcentagem e intensidade); (3) o tratamento agudo ex vivo com diazepam...

Estudo da modulação de funções efetoras de neutrófilos humanos por derivados cumarínicos: avaliação do efeito biológico sobre a produção de espécies reativas de oxigênio e a desgranulação; Study of modulation of human neutrophil effector functions by coumarin derivatives: evaluation of biological effect on reactive oxygen species production and degranulation

Fuzissaki, Carolina Nakau
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Dissertação de Mestrado Formato: application/pdf
Publicado em 06/11/2009 Português
Relevância na Pesquisa
36.81%
Os neutrófilos são células fagocíticas do sistema imune inato com mecanismos especializados de digestão de patógenos, complexos imune e detritos celulares, que são mediados principalmente por espécies reativas de oxigênio (EROs) e enzimas proteolíticas. Entretanto, a ativação maciça de neutrófilos leva a uma liberação exacerbada de enzimas e EROs para o meio extracelular, o que pode ultrapassar a capacidade de defesa tecidual, composta por antioxidantes e antiproteinases, e lesar o tecido, bem como amplificar o processo inflamatório observado em algumas doenças inflamatórias, autoimunes e infecciosas. O envolvimento de neutrófilos na fisiopatologia de tais doenças tem atraído o interesse na pesquisa de novas substâncias com propriedades antioxidantes e imunomodulatórias. Neste trabalho, foi avaliado o efeito modulatório de onze derivados de cumarinas hidroxiladas e acetoxiladas sobre duas funções efetoras de neutrófilos humanos (produção de EROs e desgranulação), bem como a citotoxicidade dessas substâncias. Além disso, a relação estrutura-atividade foi analisada. Para tais investigações, o sangue venoso foi coletado de voluntários saudáveis e os neutrófilos foram isolados pelo método da gelatina. O metabolismo oxidativo dos neutrófilos foi desencadeado por zimosan opsonizado com soro humano normal (ZIops) ou forbol-12-miristato-13-acetato (PMA)...

Macrophages and mast cells control the neutrophil migration induced by dentin proteins

Silva, T. A.; Lara, V. S.; Silva, J. S.; Oliveira, SHP; Butler, W. T.; Cunha, F. Q.
Fonte: Int Amer Assoc Dental Researchi Publicador: Int Amer Assoc Dental Researchi
Tipo: Artigo de Revista Científica Formato: 79-83
Português
Relevância na Pesquisa
36.79%
Dentin sialoprotein (DSP) and dentin phosphoprotein (DPP), the major dentin proteins, have been shown to induce neutrophil migration through release of IL-1beta, TNF-alpha, MIP-2, and KC. However, the sources of these mediators were not determined. Here, the roles of macrophages and mast cells (MC) in dentin-induced neutrophil accumulation were investigated. Peritoneal MC depletion or the enhancement of macrophage population increased DSP- and DPP-induced neutrophil extravasation. Moreover, supernatants from DSP- and DPP-stimulated macrophages caused neutrophil migration. The release of neutrophil chemotactic factor by macrophages was inhibited by dexamethasone or the supernatant of DSP- treated MC. Consistently, dexamethasone and the MC supernatant inhibited the production of IL-1beta, TNF-alpha, and MIP-2 by macrophages. This inhibitory activity of the DSP- stimulated MC was neutralized by anti-IL-4 and anti-IL-10 antibodies. These results indicate that dentin induces the release of the neutrophil chemotactic substance(s) by macrophages, which are down-modulated by MC-derived IL-4 and IL-10.

Neutrophil migration induced by IL-1β depends upon LTB4 released by macrophages and upon TNF-α and IL-1β released by mast cells

Oliveira, S. H P; Canetti, C.; Ribeiro, R. A.; Cunha, F. Q.
Fonte: Universidade Estadual Paulista Publicador: Universidade Estadual Paulista
Tipo: Artigo de Revista Científica Formato: 36-46
Português
Relevância na Pesquisa
36.85%
In the present study, we investigate whether mast cells and macrophages are involved in the control of IL-1β-induced neutrophil migration, as well as the participation of chemotactic mediators. IL-1β induced a dose-dependent neutrophil migration to the peritoneal cavity of rats which depends on LTB 4, PAF and cytokines, since the animal treatment with inhibitors of these mediators (MK 886, PCA 4248 and dexamethasone respectively) inhibited IL-1β-induced neutrophil migration. The neutrophil migration induced by IL-1β is dependent on mast cells and macrophages, since depletion of mast cells reduced the process whereas the increase of macrophage population enhanced the migration. Moreover, mast cells or macrophages stimulated with IL-1β released a neutrophil chemotactic factor, which mimicked the neutrophil migration induced by IL-1β. The chemotactic activity of the supernatant of IL-1β-stimulated macrophages is due to the presence of LTB4, since MK 886 inhibited its release. Moreover, the chemotactic activity of IL-1β-stimulated mast cells supernatant is due to the presence of IL-1β and TNF-α, since antibodies against these cytokines inhibited its activity. Furthermore, significant amounts of these cytokines were detected in the supernatant. In conclusion...

Neutrophil dysfunction varies with the stage of canine visceral leishmaniosis

Almeida, B. F M; Narciso, L. G.; Bosco, A. M.; Pereira, P. P.; Braga, E. T.; Avanço, S. V.; Marcondes, M.; Ciarlini, P. C.
Fonte: Universidade Estadual Paulista Publicador: Universidade Estadual Paulista
Tipo: Artigo de Revista Científica Formato: 6-12
Português
Relevância na Pesquisa
36.79%
Canine visceral leishmaniosis (CVL) causes a dependent-stage alteration in neutrophil oxidative metabolism. When production of reactive oxygen species (ROS) exceeds the antioxidant capacity of neutrophils, apoptosis is triggered, impairing the viability and function of these cells, which can predispose dogs to infection. However, the uremic condition observed in late-stage CVL can also alter the viability and function of human neutrophils. To more clearly understand this relationship, the apoptosis rate and oxidative metabolism of neutrophils from control dogs (n= 20) were compared to dogs in moderate (n= 15) and very severe (n= 15) stage CVL, classified according to LeishVet Consensus. To assess neutrophil oxidative metabolism, superoxide production was measured using the nitroblue tetrazolium reduction test (NBT) in isolated neutrophils. The apoptosis rate of neutrophils was estimated using the morphological method. Moderate-stage dogs presented increased superoxide production, while dogs with very severe stage CVL presented decreased superoxide production and an increase neutrophil apoptosis rate. Leishmaniosis causes differential neutrophil dysfunction according to disease stage. In moderate stage CVL, increased superoxide production is observed with no change in neutrophil viability. However...

Human neutrophil alloantigens systems

Moritz,Elyse; Norcia,Ângela M. M. I.; Cardone,José D. B.; Kuwano,Sachie T.; Chiba,Akemi K.; Yamamoto,Mihoko; Bordin,José O.
Fonte: Academia Brasileira de Ciências Publicador: Academia Brasileira de Ciências
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/09/2009 Português
Relevância na Pesquisa
36.79%
Neutrophil alloantigens are involved in a variety of clinical conditions including immune neutropenias, transfusion-related acute lung injury (TRALI), refractoriness to granulocyte transfusions and febrile transfusion reactions. In the last decade, considerable progress has been made in the characterization of the implicated antigens. Currently, seven antigens are assigned to five human neutrophil antigen (HNA) systems. The HNA-1a, HNA-1b and HNA-1c antigens have been identified as polymorphic forms of the neutrophil Fcγ receptor IIIb (CD16b), encoded by three alleles. Recently, the primary structure of the HNA-2a antigen was elucidated and the HNA-2a-bearing glycoprotein was identified as a member of the Ly-6/uPAR superfamily, which has been clustered as CD177. The HNA-3a antigen is located on a 70-95 kDa glycoprotein; however, its molecular basis is still unknown. Finally, the HNA-4a and HNA-5a antigens were found to be caused by single nucleotide mutations in the αM (CD11b) and αL (CD11a) subunits of the leucocyte adhesion molecules (β2 integrins). Molecular and biochemical characterization of neutrophil antigenshave expanded our diagnostic tools by the introduction of genotyping techniques and immunoassays for antibody identification. Further studies in the field of neutrophil immunology will facilitate the prevention and management of transfusion reactions and immune diseases caused by neutrophil antibodies.

Failure of neutrophil migration toward infectious focus in severe sepsis: a critical event for the outcome of this syndrome

Alves-Filho,José Carlos; Benjamim,Claudia; Tavares-Murta,Beatriz Martins; Cunha,Fernando Q
Fonte: Instituto Oswaldo Cruz, Ministério da Saúde Publicador: Instituto Oswaldo Cruz, Ministério da Saúde
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/03/2005 Português
Relevância na Pesquisa
36.83%
Sepsis is a systemic inflammatory response commonly caused by bacterial infection. We demonstrated that the outcome of sepsis induced by cecal ligation and puncture (CLP) correlates with the severity of the neutrophil migration failure towards infectious focus. Failure appears to be due to a decrease in the rolling and adhesion of neutrophil to endothelium cells. It seems that neutrophil migration impairment is mediated by the circulating inflammatory cytokines, such as TNF-alpha and IL-8, which induce the nitric oxide (NO) production systemically. It is supported by the fact that intravenous administration of these cytokines reduces the neutrophil migration induced by different inflammatory stimuli, and in severe sepsis the circulating concentrations of the cytokines and chemokines are significantly increased. Moreover, the neutrophil migration failure and the reduction in the rolling/adhesion were not observed in iNOS-/- mice and, aminoguanidine prevented this event. We also demonstrated that the failure of neutrophil migration is a Toll-4 receptor (TLR4) dependent mechanism, since it was not observed in TLR4 deficient mice. Furthermore, it was also observed that circulating neutrophils obtained from septic patients present failure of neutrophil chemotaxis toward fMLP...

Post-treatment neutrophil-lymphocyte ratio independently predicts amputation in critical limb ischemia without operation

Luo,Han; Yuan,Ding; Yang,Hongliu; Yukui,Ma; Huang,Bin; Yang,Yi; Xiong,Fei; Zeng,Guojun; Wu,Zhoupeng; Chen,Xiyang; Wang,Tiehao; Luo,Hailong; Zhao,Jichun
Fonte: Faculdade de Medicina / USP Publicador: Faculdade de Medicina / USP
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/04/2015 Português
Relevância na Pesquisa
36.87%
OBJECTIVES: Limited information is available concerning the post-treatment neutrophil-lymphocyte ratio in critical limb ischemia patients who receive conservative therapy. Accordingly, this study was designed to evaluate the predictive value of the post-treatment neutrophil-lymphocyte ratio in critical limb ischemia patients without surgery. METHOD: From January 2009 to January 2011, critical limb ischemia patients were admitted to a vascular center. The demographic data, patient histories, comorbidities and risk factors were documented, and the differential cell count was determined at admission and seven days later after conservative therapy. The cutoff value of the post-treatment neutrophil-lymphocyte ratio was determined by an ROC curve. Patients were divided into groups A and B according to the cutoff value. Amputation-free survival was compared between groups. Univariate and multivariate analyses were used to identify independent risk factors. RESULT: A total of 172 patients were identified with a mean age 71.98±10.09 years; among them, 122 were male. A value of 3.8 was identified as the cutoff value of the post-treatment neutrophil-lymphocyte ratio. Groups A (post-treatment neutrophil-lymphocyte ratio ≥3.8) and B (post-treatment neutrophil-lymphocyte ratio <3.8) showed a significant difference in amputation-free survival (P<0.001). The 1-year...

Quantitative methods for understanding physical mechanisms of neutrophil adhesion

Gaborski, Thomas R. (1980 - ); McGrath, James L. ; Waugh, Richard E.
Fonte: University of Rochester Publicador: University of Rochester
Tipo: Tese de Doutorado Formato: Number of Pages:xiv, 154 leaves
Português
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Thesis (Ph. D.)--University of Rochester. Dept. of Biomedical Engineering, 2008.; During inflammation, neutrophils first roll and then firmly adhere to activated endothelium in a sequence known as the adhesion cascade. Knowing the mobility and localization of the receptors that mediate binding between endothelium and neutrophils is key to building an accurate biophysical model of the adhesion cascade. The objective of this thesis is to characterize the mobility and localization of the main neutrophil adhesion receptors involved in the rolling and firm arrest stages of neutrophil recruitment To measure the natural movements of neutrophil membrane receptors, we built a novel fluorescence recovery after photobleaching (FRAP) experimental system and developed a set of complementary analytical tools to interpret data. Experiments examined non-activated neutrophils in their normal, spherical morphology. Prior studies have been performed on artificially flattened cells to accommodate the requirements of established methods for measuring diffusion of membrane proteins. Further, our studies are the first to measure the mobility of all four neutrophil receptors involved in early adhesion: the rolling associated adhesion molecules L-selectin and PSGL-1...

A kinetic model of bone marrow neutrophil production that characterizes late phenotypic maturation

Orr, Y.; Wilson, D.; Taylor, J.; Bannon, P.; Geczy, C.; Davenport, M.; Kritharides, L.
Fonte: Amer Physiological Soc Publicador: Amer Physiological Soc
Tipo: Artigo de Revista Científica
Publicado em //2007 Português
Relevância na Pesquisa
36.81%
Acute inflammatory stimuli rapidly mobilize neutrophils from the bone marrow by shortening postmitotic maturation time and releasing younger neutrophils; however, the kinetics of this change in maturation time remains unknown. We propose a kinetic model that examines the rate of change in neutrophil average age at exit from the bone marrow during active mobilization to quantify this response and use this model to examine the temporal profile of late neutrophil phenotypic maturation. Total and CD10–/CD16low circulating neutrophils were quantified in cardiac surgery patients during extracorporeal circulation (ECC). Net growth in the circulating neutrophil pool occurred during the procedural (0.04 ± 0.02 x 109·l–1·min–1), warming (0.14 ± 0.02 x 109·l–1·min–1), and weaning (0.12 ± 0.06 x 109·l–1·min–1) phases of ECC. When applied to our differential equation mathematical model, these results predict that neutrophil average age at exit from the bone marrow decreased continually during ECC, resulting in average neutrophil release 8.44 ± 2.20 h earlier during the weaning phase than at the beginning of ECC sampling. Modeling of concurrent changes in CD10–/CD16low neutrophil numbers indicates that CD10 expression is directly related to neutrophil mean age and predicts that the proportion of mobilizable postmitotic neutrophils that are CD10+ increases from 64 to 81% during these sampled 8.4 h of maturation.; Yishay Orr...

A novel proinflammatory role for annexin A1 in neutrophil transendothelial migration.

Williams, Samantha Louise
Fonte: Universidade de Adelaide Publicador: Universidade de Adelaide
Tipo: Tese de Doutorado
Publicado em //2009 Português
Relevância na Pesquisa
36.88%
Neutrophil extravasation into tissues is an essential process required for the inflammatory response. Upon receiving an inflammatory cue, neutrophils begin accumulating on the luminal surface of the endothelium. Neutrophil recruitment is initiated by selectin-mediated tethering and rolling of neutrophils along the endothelial monolayer, followed by integrin-mediated firm adhesion. Adherent neutrophils then traverse the endothelium in a process known as transendothelial migration. The events mediating the rolling and adhesion steps are well characterised, but research into the molecular mechanisms regulating transendothelial migration is an area of intense focus. A previous study conducted in our laboratory found that the activation of endothelial extracellular signal-regulated kinase (ERK) 1/2 was required for neutrophil transmigration. Furthermore, it was found that endothelial ERK was activated in response to a soluble protein produced by fMLP- or IL-8-stimulated neutrophils. In the present study, the soluble ERK-activating neutrophil protein was identified as annexin A1, which was selected as a possible candidate following mass spectrometry analysis of proteins secreted from activated neutrophils. Annexin A1 antibodies (Abs) were found to block endothelial ERK activation induced by conditioned medium harvested from stimulated neutrophils. Annexin A1 Abs were additionally able to inhibit neutrophil transmigration across human umbilical vein endothelial cell (HUVEC) monolayers in an in vitro transmigration assay. Following the purification of recombinant annexin A1...