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Search Results: 1 - 10 of 172028 matches for " Jesus F. Bermejo-Martin "
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Neuraminidase Antibodies and H5N1: Geographic-Dependent Influenza Epidemiology Could Determine Cross-Protection against Emerging Strains
Jesus F Bermejo-Martin,David J Kelvin,Yi Guan,Honglin Chen,Pilar Perez-Bre?a,Inmaculada Casas,Eduardo Arranz,Raul O de Lejarazu
PLOS Medicine , 2007, DOI: 10.1371/journal.pmed.0040212
Imbalanced pro- and anti-Th17 responses (IL-17/granulocyte colony-stimulating factor) predict fatal outcome in 2009 pandemic influenza
Raquel Almansa, Lorenzo Socias, Paula Ramirez, Ignacio Martin-Loeches, Jordi Vallés, Ana Loza, Jordi Rello, David J Kelvin, Cristobal León, Jesús Blanco, David Andaluz, Dariela Micheloud, Enrique Maraví, Raul Ortiz de Lejarazu, Jesus F Bermejo-Martin
Critical Care , 2011, DOI: 10.1186/cc10426
Abstract: In the present work, we re-analyzed the results from two cohorts of critically ill patients suffering from pandemic influenza infection in 2009 [1,2]. Thirty-five critically ill patients hospitalized with primary viral pneumonia were included in the analysis.The levels of 27 cytokines in peripheral blood measured during the first 24 hours following admission to the hospital were included in a Cox regression analysis to evaluate their association with mortality at 28 days. This analysis was adjusted by APACHE II score and the presence/absence of mechanical ventilation in order to preclude their potential influence on the results. IL-6, IL-8, IL-7, IL-17, and granulocyte colony-stimulating factor (G-CSF) yielded P-values <0.2 in the univariate analysis. In the multivariate analysis, high IL-17 levels were associated with increased probability of survival, while high levels of G-CSF were associated with increased risk of mortality at 28 days (P < 0.05; Figure 1). Kaplan Meier curves confirmed the association of IL-17 with survival and of G-CSF with occurrence of earlier death (Figure 1). Patients who died had significantly higher levels of G-CSF than those who survived (mean (standard deviation) pg/ml: 6,709.4 (17,979.1) and 2,043.9 (7,362.7), respectively; Mann Whitney U test); in contrast, surviving patients had higher levels of IL-17 than those who died (mean (standard deviation) pg/ml: 7.7 (8.1) and 1.5 (0.3), respectively; Mann Whitney U test).A beneficial role of IL-17 in lethal influenza has been previously proposed [3]. In our experience, 9 out of the 10 patients who died had undetectable levels of IL-17. G-CSF is the principal cytokine controlling neutrophil development and function and could thus mediate excessive recruitment of neutrophils to the lungs, contributing to impairment of the respiratory system. In turn, G-CSF induces overexpression of negative regulators of Th17 differentiation [5]. In fact, G-CSF levels correlated negatively with IL-17 levels in
Inflammatory Cytokine Expression Is Associated with Chikungunya Virus Resolution and Symptom Severity
Alyson A. Kelvin ,David Banner,Giuliano Silvi,Maria Luisa Moro,Nadir Spataro,Paolo Gaibani,Francesca Cavrini,Anna Pierro,Giada Rossini,Mark J. Cameron,Jesus F. Bermejo-Martin,Stéphane G. Paquette,Luoling Xu,Ali Danesh,Amber Farooqui,Ilaria Borghetto,David J. Kelvin,Vittorio Sambri,Salvatore Rubino
PLOS Neglected Tropical Diseases , 2011, DOI: 10.1371/journal.pntd.0001279
Abstract: The Chikungunya virus infection zones have now quickly spread from Africa to parts of Asia, North America and Europe. Originally thought to trigger a disease of only mild symptoms, recently Chikungunya virus caused large-scale fatalities and widespread economic loss that was linked to recent virus genetic mutation and evolution. Due to the paucity of information on Chikungunya immunological progression, we investigated the serum levels of 13 cytokines/chemokines during the acute phase of Chikungunya disease and 6- and 12-month post-infection follow-up from patients of the Italian outbreak. We found that CXCL9/MIG, CCL2/MCP-1, IL-6 and CXCL10/IP-10 were significantly raised in the acute phase compared to follow-up samples. Furthermore, IL-1β, TNF-α, Il-12, IL-10, IFN-γ and IL-5 had low initial acute phase levels that significantly increased at later time points. Analysis of symptom severity showed association with CXCL9/MIG, CXCL10/IP-10 and IgG levels. These data give insight into Chikungunya disease establishment and subsequent convalescence, which is imperative to the treatment and containment of this quickly evolving and frequently re-emerging disease.
Critical COPD respiratory illness is linked to increased transcriptomic activity of neutrophil proteases genes
Raquel Almansa, Lorenzo Socias, Monica Sanchez-Garcia, Ignacio Martín-Loeches, Milagros del Olmo, David Andaluz-Ojeda, Felipe Bobillo, Lucia Rico, Agueda Herrero, Vicente Roig, C San-Jose, Sara Rosich, Julia Barbado, Carlos Disdier, Raúl de Lejarazu, Maria C Gallegos, Victoria Fernandez, Jesus F Bermejo-Martin
BMC Research Notes , 2012, DOI: 10.1186/1756-0500-5-401
Abstract: By using Agilent microarray chips, we have profiled gene expression signatures in the whole blood of 28 COPD patients hospitalized with different degrees of respiratory compromise.12 of them needed of admission to the ICU, whilst 16 were admitted to the Respiratory Medicine Service. GeneSpring GX 11.0 software was used for performing statistical comparisons of transcript levels between ICU and non-ICU patients. Ingenuity pathway analysis 8.5 (IPA) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to select, annotate and visualize genes by function and pathway (gene ontology). T-test showed evidence of 1501 genes differentially expressed between ICU and non-ICU patients. IPA and KEGG analysis of the most representative biological functions revealed that ICU patients had increased levels of neutrophil gene transcripts, being [cathepsin G (CTSG)], [elastase, neutrophil expressed (ELANE)], [proteinase 3 (PRTN3)], [myeloperoxidase (MPO)], [cathepsin D (CTSD)], [defensin, alpha 3, neutrophil-specific (DEFA3)], azurocidin 1 (AZU1)], and [bactericidal/permeability-increasing protein (BPI)] the most representative ones. Proteins codified by these genes form part of the azurophilic granules of neutrophils and are involved in both antimicrobial defence and tissue damage. This “neutrophil signature” was paralleled by the necessity of advanced respiratory and vital support, and the presence of bacterial infection.Study of transcriptomic signatures in blood suggests an essential role of neutrophil proteases in COPD patients with critical respiratory illness. Measurement and modulation of the expression of these genes could present an option for clinical monitoring and treatment of severe COPD exacerbations.Patients with Chronic Obstructive Pulmonary Disease (COPD) suffer from periodical exacerbations, characterized by recurrent episodes of worsening respiratory symptoms. Exacerbations result in further decreases in lung function, impairing the patient’s quality of
Interleukin-6 Is a Potential Biomarker for Severe Pandemic H1N1 Influenza A Infection
Stéphane G. Paquette, David Banner, Zhen Zhao, Yuan Fang, Stephen S. H. Huang, Alberto J. Le?n, Derek C. K. Ng, Raquel Almansa, Ignacio Martin-Loeches, Paula Ramirez, Lorenzo Socias, Ana Loza, Jesus Blanco, Paola Sansonetti, Jordi Rello, David Andaluz, Bianche Shum, Salvatore Rubino, Raul Ortiz de Lejarazu, Dat Tran, Giovanni Delogu, Giovanni Fadda, Sigmund Krajden, Barry B. Rubin, Jesús F. Bermejo-Martin, Alyson A. Kelvin, David J. Kelvin
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0038214
Abstract: Pandemic H1N1 influenza A (H1N1pdm) is currently a dominant circulating influenza strain worldwide. Severe cases of H1N1pdm infection are characterized by prolonged activation of the immune response, yet the specific role of inflammatory mediators in disease is poorly understood. The inflammatory cytokine IL-6 has been implicated in both seasonal and severe pandemic H1N1 influenza A (H1N1pdm) infection. Here, we investigated the role of IL-6 in severe H1N1pdm infection. We found IL-6 to be an important feature of the host response in both humans and mice infected with H1N1pdm. Elevated levels of IL-6 were associated with severe disease in patients hospitalized with H1N1pdm infection. Notably, serum IL-6 levels associated strongly with the requirement of critical care admission and were predictive of fatal outcome. In C57BL/6J, BALB/cJ, and B6129SF2/J mice, infection with A/Mexico/4108/2009 (H1N1pdm) consistently triggered severe disease and increased IL-6 levels in both lung and serum. Furthermore, in our lethal C57BL/6J mouse model of H1N1pdm infection, global gene expression analysis indicated a pronounced IL-6 associated inflammatory response. Subsequently, we examined disease and outcome in IL-6 deficient mice infected with H1N1pdm. No significant differences in survival, weight loss, viral load, or pathology were observed between IL-6 deficient and wild-type mice following infection. Taken together, our findings suggest IL-6 may be a potential disease severity biomarker, but may not be a suitable therapeutic target in cases of severe H1N1pdm infection due to our mouse data.
Host adaptive immunity deficiency in severe pandemic influenza
Jesus F Bermejo-Martin, Ignacio Martin-Loeches, Jordi Rello, Andres Antón, Raquel Almansa, Luoling Xu, Guillermo Lopez-Campos, Tomás Pumarola, Longsi Ran, Paula Ramirez, David Banner, Derek Cheuk Ng, Lorenzo Socias, Ana Loza, David Andaluz, Enrique Maravi, Maria J Gómez-Sánchez, Mónica Gordón, Maria C Gallegos, Victoria Fernandez, Sara Aldunate, Cristobal León, Pedro Merino, Jesús Blanco, Fernando Martin-Sanchez, Lucia Rico, David Varillas, Veronica Iglesias, Maria ángeles Marcos, Francisco Gandía
Critical Care , 2010, DOI: 10.1186/cc9259
Abstract: We utilized gene expression, cytokine profiles and generation of antibody responses following hospitalization in 19 critically ill patients with primary pandemic A/H1N1/2009 influenza pneumonia for identifying host immune responses associated with clinical outcome. Ingenuity pathway analysis 8.5 (IPA) (Ingenuity Systems, Redwood City, CA) was used to select, annotate and visualize genes by function and pathway (gene ontology). IPA analysis identified those canonical pathways differentially expressed (P < 0.05) between comparison groups. Hierarchical clustering of those genes differentially expressed between groups by IPA analysis was performed using BRB-Array Tools v.3.8.1.The majority of patients were characterized by the presence of comorbidities and the absence of immunosuppressive conditions. pH1N1 specific antibody production was observed around day 9 from disease onset and defined an early period of innate immune response and a late period of adaptive immune response to the virus. The most severe patients (n = 12) showed persistence of viral secretion. Seven of the most severe patients died. During the late phase, the most severe patient group had impaired expression of a number of genes participating in adaptive immune responses when compared to less severe patients. These genes were involved in antigen presentation, B-cell development, T-helper cell differentiation, CD28, granzyme B signaling, apoptosis and protein ubiquitination. Patients with the poorest outcomes were characterized by proinflammatory hypercytokinemia, along with elevated levels of immunosuppressory cytokines (interleukin (IL)-10 and IL-1ra) in serum.Our findings suggest an impaired development of adaptive immunity in the most severe cases of pandemic influenza, leading to an unremitting cycle of viral replication and innate cytokine-chemokine release. Interruption of this deleterious cycle may improve disease outcome.Pandemic 2009 influenza A(H1N1)(p2009A(H1N1)) viral infections continues
Direct association between pharyngeal viral secretion and host cytokine response in severe pandemic influenza
Raquel Almansa, Andres Anton, Paula Ramirez, Ignacio Martin-Loeches, David Banner, Tomás Pumarola, Luoling Xu, Jesús Blanco, Longsi Ran, Guillermo Lopez-Campos, Fernando Martin-Sanchez, Lorenzo Socias, Ana Loza, David Andaluz, Enrique Maravi, Mónica Gordón, Maria C Gallegos, Victoria Fernandez, Cristobal León, Pedro Merino, Maria Marcos, Francisco Gandía, Felipe Bobillo, Salvador Resino, Jose Ma Eiros, Carmen Castro, Paula Mateo, Milagros Gonzalez-Rivera, Jordi Rello, Raul de Lejarazu, David J Kelvin, Jesus F Bermejo-Martin
BMC Infectious Diseases , 2011, DOI: 10.1186/1471-2334-11-232
Abstract: Twenty three patients admitted to the ICU with primary viral pneumonia were included in this study. A quantitative PCR based method targeting the M1 influenza gene was developed to quantify pharyngeal viral load. In addition, by using a multiplex based assay, we systematically evaluated host cytokine responses to the viral infection at admission to the ICU. Correlation studies between cytokine levels and viral load were done by calculating the Spearman correlation coefficient.Fifteen patients needed of intubation and ventilation, while eight did not need of mechanical ventilation during ICU hospitalization. Viral load in pharyngeal swabs was 300 fold higher in the group of patients with the worst respiratory condition at admission to the ICU. Pharyngeal viral load directly correlated with plasma levels of the pro-inflammatory cytokines IL-6, IL-12p70, IFN-γ, the chemotactic factors MIP-1β, GM-CSF, the angiogenic mediator VEGF and also of the immuno-modulatory cytokine IL-1ra (p < 0.05). Correlation studies demonstrated also the existence of a significant positive association between the levels of these mediators, evidencing that they are simultaneously regulated in response to the virus.Severe respiratory disease caused by the 2009 pandemic influenza virus is characterized by the existence of a direct association between viral replication and host cytokine response, revealing a potential pathogenic link with the severe disease caused by other influenza subtypes such as H5N1.Two years later, the pathogenesis of the illness caused by 2009 pandemic influenza is still poorly known. Pregnancy, severe obesity, cardiovascular disease and diabetes have been reported as risk factors for critical illness following infection with the pandemic virus [1,2]. Persistence of viral secretion has been found in the patients with the worst outcomes [3-5]. Prompt antiviral treatment has been recognized as a protective factor [6]. A number of studies report increased and persistent level
Th1 and Th17 hypercytokinemia as early host response signature in severe pandemic influenza
Jesus F Bermejo-Martin, Raul Ortiz de Lejarazu, Tomas Pumarola, Jordi Rello, Raquel Almansa, Paula Ramírez, Ignacio Martin-Loeches, David Varillas, Maria C Gallegos, Carlos Serón, Dariela Micheloud, Jose Manuel Gomez, Alberto Tenorio-Abreu, María J Ramos, M Lourdes Molina, Samantha Huidobro, Elia Sanchez, Mónica Gordón, Victoria Fernández, Alberto del Castillo, Ma ángeles Marcos, Beatriz Villanueva, Carlos Javier López, Mario Rodríguez-Domínguez, Juan-Carlos Galan, Rafael Cantón, Aurora Lietor, Silvia Rojo, Jose M Eiros, Carmen Hinojosa
Critical Care , 2009, DOI: 10.1186/cc8208
Abstract: We profiled 29 cytokines and chemokines and evaluated the haemagglutination inhibition activity as quantitative and qualitative measurements of host immune responses in serum obtained during the first five days after symptoms onset, in two cohorts of nvH1N1 infected patients. Severe patients required hospitalization (n = 20), due to respiratory insufficiency (10 of them were admitted to the intensive care unit), while mild patients had exclusively flu-like symptoms (n = 15). A group of healthy donors was included as control (n = 15). Differences in levels of mediators between groups were assessed by using the non parametric U-Mann Whitney test. Association between variables was determined by calculating the Spearman correlation coefficient. Viral load was performed in serum by using real-time PCR targeting the neuraminidase gene.Increased levels of innate-immunity mediators (IP-10, MCP-1, MIP-1β), and the absence of anti-nvH1N1 antibodies, characterized the early response to nvH1N1 infection in both hospitalized and mild patients. High systemic levels of type-II interferon (IFN-γ) and also of a group of mediators involved in the development of T-helper 17 (IL-8, IL-9, IL-17, IL-6) and T-helper 1 (TNF-α, IL-15, IL-12p70) responses were exclusively found in hospitalized patients. IL-15, IL-12p70, IL-6 constituted a hallmark of critical illness in our study. A significant inverse association was found between IL-6, IL-8 and PaO2 in critical patients.While infection with the nvH1N1 induces a typical innate response in both mild and severe patients, severe disease with respiratory involvement is characterized by early secretion of Th17 and Th1 cytokines usually associated with cell mediated immunity but also commonly linked to the pathogenesis of autoimmune/inflammatory diseases. The exact role of Th1 and Th17 mediators in the evolution of nvH1N1 mild and severe disease merits further investigation as to the detrimental or beneficial role these cytokines play in severe i
Intubated patients developing tracheobronchitis or pneumonia have distinctive complement system gene expression signatures in the pre-infection period: A pilot study
Martín-Loeches,I.; Papiol,E.; Almansa,R.; López-Campos,G.; Bermejo-Martin,J.F.; Rello,J.;
Medicina Intensiva , 2012,
Abstract: introduction: it remains unknown why some intubated patients remain infection-free while others develop tracheobronchitis (vat) or pneumonia (vap). objective: to identify and compare vap/vat gene expression "signatures" using genome-wide oligonucleotide microarrays. material and methods: a prospective translational study of gene expression profiles of vap and vat groups was carried out, establishing comparisons in both pre-infection and infection phases. pathway and functional analyses were performed with ingenuity pathway analysis (ipa). data analysis and hierarchical clustering of the genes involved in the signalling pathways expressed differentially in the two groups were performed with genespring gx 11.0. results: eight patients developing respiratory infections (3 vap and 5 vat) after 4 days of mechanical ventilation were assessed. comparison of gene expression profiles in the pre-infection period revealed 5595 genes expressed differentially between vap and vat (p<0.01, fold change >2). comparative ipa analysis identified a significant depression of the complement system signalling pathway in the vap group, affecting the classical pathway along with the final common pathway (p<0.05). in addition, the camp and calcium signalling pathways were also significantly depressed in the vap group during the pre-infection phase also. conclusion: intubated patients complicated with pneumonia developed immune impairment in the pre-infection period, manifesting as a relatively lower expression of genes involved in the complement system that differed from patients developing tracheobronchitis. these findings suggest that a significant proportion of vap episodes cannot be prevented, but might be treatable through pre-emptive therapy.
Pandemic and post-pandemic Influenza A (H1N1) infection in critically ill patients
Ignacio Martin-Loeches, Emili Díaz, Loreto Vidaur, Antoni Torres, Cesar Laborda, Rosa Granada, Juan Bonastre, Mar Martín, Josu Insausti, Angel Arenzana, Jose Guerrero, Ines Navarrete, Jesus Bermejo-Martin, David Suarez, Alejandro Rodriguez, the H1N1 SEMICYUC/REIPI/CIBERES Working group
Critical Care , 2011, DOI: 10.1186/cc10573
Abstract: A prospective, observational, multi-center study was carried out to evaluate the clinical characteristics and demographics of patients with positive RT-PCR for H1N1 admitted to 148 Spanish intensive care units (ICUs). Data were obtained from the 2009 pandemic and compared to the 2010-2011 post-pandemic period.Nine hundred and ninety-seven patients with confirmed An/H1N1 infection were included. Six hundred and forty-eight patients affected by 2009 (pH1N1) virus infection and 349 patients affected by the post-pandemic Influenza (H1N1)v infection period were analyzed. Patients during the post-pandemic period were older, had more chronic comorbid conditions and presented with higher severity scores (Acute Physiology And Chronic Health Evaluation II (APACHE II) and Sequential Organ Failure Assessment (SOFA)) on ICU admission. Patients from the post-pandemic Influenza (H1N1)v infection period received empiric antiviral treatment less frequently and with delayed administration. Mortality was significantly higher in the post-pandemic period. Multivariate analysis confirmed that haematological disease, invasive mechanical ventilation and continuous renal replacement therapy were factors independently associated with worse outcome in the two periods. HIV was the only new variable independently associated with higher ICU mortality during the post-pandemic Influenza (H1N1)v infection period.Patients from the post-pandemic Influenza (H1N1)v infection period had an unexpectedly higher mortality rate and showed a trend towards affecting a more vulnerable population, in keeping with more typical seasonal viral infection.There is a vast amount of information published regarding the impact of the 2009 pandemic Influenza A (H1N1)v infection [1,2]. The pandemic represented a challenge for physicians worldwide, manifesting with the acute onset of respiratory failure in a patient population often young, with few comorbid conditions. Several recommendations have been considered, taking i
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