Un rol para Th17 en las enfermedades respiratorias

Las células T-helper 17 (Th17) son un nuevo subconjunto de las células T-helper CD4 , caracterizadas principalmente por la producción de interleuquina 17 (IL-17A). Las funciones de las células Th17 en numerosas enfermedades infecciosas y autoinmunes han comenzado a ser clarificadas. La respuesta Th17 es importante en la defensa contra muchos microorganismos, pero también pueden contribuir a la inmunopatología. Este trabajo presenta los avances en el tema.T-helper 17 (Th17) cells are a new CD4 helper subset mainly characterized by interleukin 17 (IL-17A) production. The functions of Th17 cells in several infectious and autoimmune diseases have recently started to be clarified. Th17 immune response is important for the defense against many microorganisms but they can also contribute to immunopathology. This work presents the new advances in the field.Fil: Acosta, Patricio Leandro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Brief History and Characterization of Enhanced Respiratory Syncytial Virus Disease

In 1967, infants and toddlers immunized with a formalin-inactivated vaccine against respiratory syncytial virus (RSV) experienced an enhanced form of RSV disease characterized by high fever, bronchopneumonia, and wheezing when they became infected with wild-type virus in the community. Hospitalizations were frequent, and two immunized toddlers died upon infection with wild-type RSV. The enhanced disease was initially characterized as a "peribronchiolar monocytic infiltration with some excess in eosinophils." Decades of research defined enhanced RSV disease (ERD) as the result of immunization with antigens not processed in the cytoplasm, resulting in a nonprotective antibody response and CD4(+) T helper priming in the absence of cytotoxic T lymphocytes. This response to vaccination led to a pathogenic Th2 memory response with eosinophil and immune complex deposition in the lungs after RSV infection. In recent years, the field of RSV experienced significant changes. Numerous vaccine candidates with novel designs and formulations are approaching clinical trials, defying our previous understanding of favorable parameters for ERD. This review provides a succinct analysis of these parameters and explores criteria for assessing the risk of ERD in new vaccine candidates.Fil: Acosta, Patricio Leandro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fundación Infant; ArgentinaFil: Caballero, Mauricio Tomás. Fundación Infant; ArgentinaFil: Polack, Fernando Pedro. University Medical Center; Estados Unidos. Fundación Infant; Argentin

Respiratory failure and death in vulnerable premature children with lower respiratory tract illness

Background. Efforts to better understand the risk factors associated with respiratory failure (RF) and fatal lower respiratory tract infection (LRTI) in premature children in developing countries are necessary to elaborate evidenced-based preventive interventions. We aim to characterize the burden of respiratory syncytial virus (RSV) and human metapneumovirus (hMPV) LRTI in premature children and determine risk factors for RF and fatal illness in a vulnerable population. Methods. This is a prospective, population-based, cross-sectional study. Subjects with severe LRTI were enrolled during respiratory season. Risk factors for RF and death in premature infants were investigated. Results. A total of 664 premature children participated. Infant's hospitalization rate due to LRTI was 82.6/1000 (95% confidence interval [CI], 68.6-96.7/1000). Infant's RSV and hMPV rates were 40.9/1000 (95% CI, 36.3-45.6/1000) and 6.6/1000 (95% CI, 3.9- 9.2/1000), respectively. The RF rate was 8.2/1000 (95% CI, 4.9-11.5/1000). The LRTI mortality was 2.2/1000 (95% CI, 0.7-3.7/1000); for RSV, the rate was 0.8/1000 (95% CI, 0-1.7/1000) with a case-fatality ratio of 1.8%. Never breastfeeding, malnutrition, younger than 6 months, congenital heart disease, and lower hematocrit were risk factors for RF. Experiencing pneumonia, pneumothorax, sepsis, or apnea were clinical determinants of poor outcomes. Conclusions. Premature children under 2 years old in vulnerable environments experience RF and death more often than term counterparts. Modifiable risk factors associated with poor outcomes should prompt evidence-based interventions.Fil: Ofman, Gaston. Fundacion de Endocrinologia Infantil.; ArgentinaFil: Pradarelli, Brad. Fundacion de Endocrinologia Infantil.; ArgentinaFil: Caballero, Mauricio Tomás. Fundacion de Endocrinologia Infantil.; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Bianchi, Alejandra. Fundacion de Endocrinologia Infantil.; ArgentinaFil: Grimaldi, Luciano Alva. Gobierno de la Provincia de Buenos Aires. Hospital Zonal General de Agudos Doctor Lucio Melendez.; ArgentinaFil: Sancilio, Andrea. Gobierno de la Provincia de Buenos Aires. Hospital Interzonal de Agudos Evita; ArgentinaFil: Duenas, Karina. Gobierno de la Provincia de Buenos Aires. Hospital Interzonal de Agudos Evita; ArgentinaFil: Rodriguez, Andrea. Gobierno de la Provincia de Buenos Aires. Hospital Provincial Evita Pueblo.; ArgentinaFil: Ferrero, Fernando. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); ArgentinaFil: Ferretti, Adrian. Fundacion de Endocrinologia Infantil.; ArgentinaFil: Coviello, Silvina Andrea. Fundacion de Endocrinologia Infantil.; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Ferolla, Fausto Martín. Fundacion de Endocrinologia Infantil.; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Acosta, Patricio Leandro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fundacion de Endocrinologia Infantil.; ArgentinaFil: Bergel, Eduardo. Fundacion de Endocrinologia Infantil.; ArgentinaFil: Libster, Romina Paula. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fundacion de Endocrinologia Infantil.; ArgentinaFil: Polack, Fernando Pedro. Fundacion de Endocrinologia Infantil.; Argentin

Role for Maternal Asthma in Severe Human Metapneumovirus Lung Disease Susceptibility in Children

Background: Severity of human metapneumovirus (hMPV) lower respiratory illness (LRTI) is considered similar to that observed for respiratory syncytial virus (RSV). However, differences in severity between these pathogens have been noted, suggesting the degree of illness may vary in different populations. Moreover, a potential association between hMPV and asthma also suggests that hMPV may preferentially affect asthmatic subjects. Methods: In a population-based surveillance study in children aged <2 years admitted for severe LRTI in Argentina, nasopharyngeal aspirates were tested by RT-PCR for hMPV, RSV, influenza A, and human rhinovirus. Results: Of 3947 children, 383 (10%) were infected with hMPV. The hospitalization rate for hMPV LRTI was 2.26 per 1000 children (95% confidence interval [CI], 2.04-2.49). Thirty-nine (10.2%) patients infected with hMPV experienced life-threatening disease (LTD; 0.23 per 1000 children; 95% CI,. 16-.31/1000), and 2 died (mortality rate 0.024 per 1000; 95% CI,. 003-.086). In hMPV-infected children birth to an asthmatic mother was an increased risk for LTD (odds ratio, 4.72; 95% CI, 1.39-16.01). We observed a specific interaction between maternal asthma and hMPV infection affecting risk for LTD. Conclusions: Maternal asthma increases the risk for LTD in children <2 years old hospitalized for severe hMPV LRTI.Fil: Libster, Romina Paula. Fundación para la Investigación en Infectología Infantil; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Esteban, Ignacio. Fundación para la Investigación en Infectología Infantil; Argentina. Gobierno de la Ciudad de Buenos Aires. Hospital de Pediatría "Juan P. Garrahan"; ArgentinaFil: Bianchi, Alejandra Silvina. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Alva Grimaldi, Luciano. Gobierno de la Provincia de Buenos Aires. Hospital Zonal General de Agudos Doctor Lucio Melendez.; ArgentinaFil: Dueñas, Karina. Gobierno de la Provincia de Buenos Aires. Hospital Interzonal de Agudos Evita.; ArgentinaFil: Sancillo, Andrea. Gobierno de la Provincia de Buenos Aires. Hospital Interzonal de Agudos Evita.; ArgentinaFil: Rodriguez, Andrea. Gobierno de la Provincia de Buenos Aires. Hospital Provincial Evita Pueblo.; ArgentinaFil: Ferrero, Fernando. Gobierno de la Ciudad de Buenos Aires. Hospital General de Niños Pedro Elizalde (ex Casa Cuna); ArgentinaFil: Stein, Katherine. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Acosta, Patricio Leandro. Fundación para la Investigación en Infectología Infantil; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Ferolla, Fausto Martín. Fundación para la Investigación en Infectología Infantil; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Bergel, Eduardo. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Caballero, Mauricio Tomás. Fundación para la Investigación en Infectología Infantil; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Polack, Fernando Pedro. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Pellegrino, Gustavo. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Fernandez Gago, Guadalupe. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Pozzolo, Cecilia. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Castro, Laura. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Almeida, Rodrigo Egues. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Rebec, Beatriz. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: González, Mariela. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Calvo, Mariel. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Henrichsen, Julieta. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Nocito, Celina. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Barbero, Guillermo. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Ves Losada, Juan. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Bonina, Angel. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Flamenco, Edgardo. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Rodriguez Perez, Alberto. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Kobylarz, Alicia. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Raggio, Mirta. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Schavlosky, Graciela. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Caria, Adriana. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Barboza, Edgar. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Sastre, Gustavo. Fundación para la Investigación en Infectología Infantil; Argentin

How can young scientists influence and shape science policy in their homes and across the globe?

Although policy making is generally thought to be the responsibility ofexperienced and senior bureaucrats, the voice of the younger generationand, in particular, the voice of early-career scientists is valuableto consider. History has repeatedly been shaped as the result of theactions of youth. Young people are among the creators of the greatreligions, the founders of civilizations, the heroes of our republics, and the innovators in the fields of art, science and technology. Take Albert Einstein, who at the age of 37, published the general theory of relativity. The energy, creativity, enthusiasm, and general open-mindedness that characterize early-career scientists equip them with the ability to pave the path for change in the area of science-based policy making, both locally and around the globe.Fil: Acosta, Patricio Leandro. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Chaganti, S.. No especifíca;Fil: Dumre, S.. No especifíca;Fil: Ezizuzor, S.. No especifíca;Fil: Karczerska Golec, J.. No especifíca;Fil: Newire, E.. No especifíca;Fil: Buhiyan, T.. No especifíca;Fil: Allibhoy, S.. No especifíca

Characterization of Type I Interferon Responses in Dengue and Severe Dengue in Children in Paraguay

Background: Infection with dengue virus (DENV) produces a wide spectrum of clinical illness ranging from asymptomatic infection to mild febrile illness, and to severe forms of the disease. Type I interferons (IFNs) represent an initial and essential host defense response against viruses. DENV has been reported to trigger a robust type I IFN response; however, IFN-α/β profile in the progression of disease is not well characterized.Objectives and study design: In this context, we conducted a retrospective study assessing the circulating serum levels of type I IFNs and related cytokines at different phases of illness in children during the 2011 outbreak of DENV in Paraguay. Demographic, clinical, laboratory and virological data were analyzed.Results: During defervescence, significantly higher levels of IFN-β, IL-6 and MIP-1β, were detected in severe vs. non-severe dengue patients. Additionally, a significant positive correlation between INF-α and viremia was detected in children with severe dengue. Significant positive correlations were also observed between IFN-β serum levels and hematocrit/hemoglobin during the febrile phase, whereas IFN-α levels negatively correlated with white blood cells during defervescence in severe dengue patients. Furthermore, previous serologic status of patients to DENV did not influence type I IFN production.Conclusions: The distinct type I IFN profile in children with dengue and severe dengue, as well as its association with viral load, cytokine production and laboratory manifestations indicate differences in innate and adaptive immune responses that should be investigated further in order to unveil the association of immunological and physiological pathways that underlie in DENV infection.Fil: Talarico, Laura Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Byrne, Alana Brooke. Fundación para la Investigación en Infectología Infantil; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Amarilla, Sara. Instituto de Medicina Tropical; Paraguay. Universidad Nacional de Asunción; ParaguayFil: Lovera, Dolores. Universidad Nacional de Asunción; Paraguay. Instituto de Medicina Tropical; ParaguayFil: Vázquez, Cynthia. Laboratorio Central de Salud Pública; ParaguayFil: Chamorro, Gustavo. Laboratorio Central de Salud Pública; ParaguayFil: Acosta, Patricio Leandro. Fundación para la Investigación en Infectología Infantil; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Ferretti, Adrián. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Caballero, Mauricio Tomás. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Arbo, Antonio. Instituto de Medicina Tropical; Paraguay. Universidad Nacional de Asunción; ParaguayFil: Polack, Fernando Pedro. Fundación para la Investigación en Infectología Infantil; Argentin

Genetic susceptibility to life-threatening respiratory syncytial virus infection in previously healthy infants

Background: Genetic background may be an important host determinant of respiratory syncytial virus (RSV) disease severity, but full characterization of susceptibility genes remains unclear. This study aimed to assess the presence of specific single-nucleotide polymorphisms (SNPs) in selected genes codifying for different components of the antiviral innate immune response, to determine their role for developing RSV life-threatening disease (LTD). Methods: Prospective cohort study including previously healthy full-term infants hospitalized with a first RSV infection during 2017-2018. RSV detection, quantification and subgroup determination, and genotyping for SNPs in Toll-like receptor 4 (TLR4 rs4986790, rs4986791), Toll-like receptor 8 (TLR8 rs3761624), macrophage receptor with collagenous structure (MARCO rs1318645) and myxovirus resistance 1 (MX1 rs469390) were performed by real-time polymerase chain reaction in nasopharyngeal aspirates obtained on admission. Patients with LTD were those admitted to the intensive care unit requiring ventilatory support. Results: Seventy-five patients were studied, 15 (20%) developed LTD. Infants with concurrent SNPs in MX1 and TLR8, MARCO and TLR8 or MARCO, MX1 and TLR8 had an increased risk of developing LTD. Multivariable logistic regression analysis confirmed this significant association (odds ratio [OR] = 3.75, P = 0.046; OR = 3.92, P = 0.040; OR = 5.56, P = 0.010, respectively). No differences were seen in viral load of patients with LTD compared with those with better outcome (P = 0.737). In addition, no differences in viral load were seen in patients with the described high-risk SNPs compared with those without these polymorphisms. Conclusions: Life-threatening RSV infection in previously healthy infants was significantly associated with the presence of combined SNPs in MARCO, MX1 and TLR8.Fil: Lopez, Eduardo Luis. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez". Departamento de Medicina; ArgentinaFil: Ferolla, Fausto Martín. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez". Departamento de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Toledano, Analia. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez". Departamento de Medicina; ArgentinaFil: Yfran, Eduardo Walter. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez". Departamento de Medicina; ArgentinaFil: Giordano, Ana Clara. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez". Departamento de Medicina; ArgentinaFil: Carrizo, Bárbara. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez". Departamento de Medicina; ArgentinaFil: Feldman, Florencia. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez". Departamento de Medicina; ArgentinaFil: Talarico, Laura Beatriz. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez". Departamento de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Caratozzolo, Ana. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez". Departamento de Medicina; ArgentinaFil: Contrini, María Marta. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez". Departamento de Medicina; ArgentinaFil: Acosta, Patricio Leandro. Gobierno de la Ciudad Autónoma de Buenos Aires. Hospital General de Niños "Ricardo Gutiérrez". Departamento de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

IL-8/IL-17 gene variations and the susceptibility to severe viral bronchiolitis

Clinical manifestations of acute bronchiolitis (AB) vary from minimal disease to severe respiratory failure. The response to respiratory viral infections is possibly influenced by genetic polymorphisms linked to the regulation of the inflammatory response. In the present study, we investigated whether interleukin-8 (IL-8) and interleukin-17 (IL-17) genetic variants are associated with the severity of AB. A group of Brazilian infants hospitalized with AB and a control group (infants with no or mild AB, without hospitalization) were genotyped for four IL-8/IL-17 variations. For replication, we studied an Argentinean population sample of infants with mild and severe AB. IL-8 polymorphism (rs 2227543) and IL-17 (rs2275913) variants showed significant associations with the severity of AB. The effect of the IL-8 variation could be replicated in the Argentinean sample. This finding suggests that IL-8 variations may influence the severity of AB in young infants. Further genetic association studies in low- or middle-income populations are necessary with the aim of expanding knowledge in this area.Fil: Pinto, L.A.. Aliança INFANT; Brasil. Pontificia Universidade Católica do Rio Grande do Sul; BrasilFil: De Azeredo Leitão, L.A.. Aliança INFANT; Brasil. Pontificia Universidade Católica do Rio Grande do Sul; BrasilFil: Mocellin, M.. Aliança INFANT; Brasil. Pontificia Universidade Católica do Rio Grande do Sul; BrasilFil: Acosta, Patricio Leandro. Aliança INFANT; Brasil. Fundación INFANT; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Caballero, Mauricio Tomás. Aliança INFANT; Brasil. Fundación INFANT; ArgentinaFil: Libster, Romina Paula. Aliança INFANT; Brasil. Fundación INFANT; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Vargas, J. E.. Aliança INFANT; Brasil. Pontificia Universidade Católica do Rio Grande do Sul; BrasilFil: Polack, F.. Aliança INFANT; Brasil. Fundación INFANT; ArgentinaFil: Comaru, T.. Aliança INFANT; Brasil. Pontificia Universidade Católica do Rio Grande do Sul; BrasilFil: Stein, R.T.. Aliança INFANT; Brasil. Pontificia Universidade Católica do Rio Grande do Sul; BrasilFil: De Souza, A.P.. Aliança INFANT; Brasil. Pontificia Universidade Católica do Rio Grande do Sul; Brasi

Protective phenotypes of club cells and alveolar macrophages are favored as part of endotoxin-mediated prevention of asthma

Atopic asthma is a chronic allergic disease that involves T-helper type 2 (Th2)-inflammation and airway remodeling. Bronchiolar club cells (CC) and alveolar macrophages (AM) are sentinel cells of airway barrier against inhaled injuries, where allergy induces mucous metaplasia of CC and the alternative activation of AM, which compromise host defense mechanisms and amplify Th2-inflammation. As there is evidence that high levels of environmental endotoxin modulates asthma, the goal of this study was to evaluate if the activation of local host defenses by Lipopolysaccharide (LPS) previous to allergy development can contribute to preserving CC and AM protective phenotypes. Endotoxin stimulus before allergen exposition reduced hallmarks of allergic inflammation including eosinophil influx, Interleukin-4 and airway hyperreactivity, while the T-helper type 1 related cytokines IL-12 and Interferon-γ were enhanced. This response was accompanied by the preservation of the normal CC phenotype and the anti-allergic proteins Club Cell Secretory Protein (CCSP) and Surfactant-D, thereby leading to lower levels of CC metaplasia and preventing the increase of the pro-Th2 cytokine Thymic stromal lymphopoietin. In addition, classically activated alveolar macrophages expressing nitric oxide were promoted over the alternatively activated ones that expressed arginase-1. We verified that LPS induced a long-term overexpression of CCSP and the innate immune markers Toll-like receptor 4, and Tumor Necrosis Factor-α, changes that were preserved in spite of the allergen challenge. These results demonstrate that LPS pre-exposition modifies the local bronchioalveolar microenvironment by inducing natural anti-allergic mechanisms while reducing local factors that drive Th2 type responses, thus modulating allergic inflammation.Fil: García, Luciana Noemí. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Cordoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Universidad Nacional de Cordoba. Facultad de Medicina. Centro de Microscopia Electronica; ArgentinaFil: Leimgruber, Carolina. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Cordoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Universidad Nacional de Cordoba. Facultad de Medicina. Centro de Microscopia Electronica; ArgentinaFil: Uribe Echevarría, E. M.. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Cordoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Universidad Nacional de Cordoba. Facultad de Medicina. Centro de Microscopia Electronica; ArgentinaFil: Acosta, Patricio Leandro. Fundación para la Investigación en Infectologia Infantil; ArgentinaFil: Brahamian, Jorge M.. Fundación para la Investigación en Infectologia Infantil; ArgentinaFil: Polack, Fernando P.. Fundación para la Investigación en Infectologia Infantil; Argentina. Vanderbilt University; Estados UnidosFil: Miró, María Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Quintar, Amado Alfredo. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Cordoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Universidad Nacional de Cordoba. Facultad de Medicina. Centro de Microscopia Electronica; ArgentinaFil: Sotomayor, Claudia Elena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Maldonado, Cristina Alicia. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnologico Cordoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Universidad Nacional de Cordoba. Facultad de Medicina. Centro de Microscopia Electronica; Argentin

Interleukin-13 associates with life-threatening rhinovirus infections in infants and young children

Objective: Delineate risk factors associated with severe hypoxemia (O2 sat ≤87%) in infants and children younger than 2 years hospitalized with single pathogen HRV infection. Study Design: Prospective study in a yearly catchment population of 56 560 children 10 pg/mL) predisposed to life-threatening disease. Conclusions: Targeted interventions against IL-13 should be evaluated to decrease severity of HRV illness in infancy and early childhood.Fil: Caballero, Mauricio Tomás. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Hijano, Diego Raúl. Fundación para la Investigación en Infectología Infantil; Argentina. St. Jude Children's Research Hospital; Estados UnidosFil: Acosta, Patricio Leandro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Mateu, Cecilia Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Marcone, Débora Natalia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Centro de Educación Médica e Investigaciones Clínicas “Norberto Quirno”; ArgentinaFil: Linder, Jodell E.. Vanderbilt University; Estados UnidosFil: Talarico, Laura Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fundación para la Investigación en Infectología Infantil; ArgentinaFil: Elder, John M.. Vanderbilt University; Estados UnidosFil: Echavarría, Marcela Silvia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Centro de Educación Médica e Investigaciones Clínicas “Norberto Quirno”; ArgentinaFil: Miller, Eva Kathryn. Vanderbilt University; Estados UnidosFil: Polack, Fernando Pedro. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fundación para la Investigación en Infectología Infantil; Argentin