Esophageal varices in patients with chronic liver disease: comparative study of predictive criteria

INTRODUCCION: Las varices esofagicas (VE) son una complicacion mayor de la hipertensión portal (HTP), su prevalencia en pacientes con hepatopatia cronica (HPC) oscila entre 60-80% y mortalidad per sangrado entre 17 y 57%. En 1996 la Asociaci6n Americana aconsej6 el screening de VE en todo paciente con HPC. Numerosos trabajos intentan descubrir variables clinicas, laboratorio o imagenes predictores de la presencia de VE para racionalizar y hacer costo efectivo el screening endoscOpico. OBJETIVO: Cuantificar y comparar la capacidad predictiva de VE de distintas variables: clinicas (Clase funcional hepatica —CFH- de Child-Pugh), de laboratorio (recuento de plaquetas), ecograficas (tamano bipolar del bazo y diametro de la vena porta) mixtas (cociente plaquetas / Bazo propuesta de Gianini).INTRODUCTION: Esophageal varices (EV)) are major complications of portal hyper¬tension (PHT)), its prevalence in patients with chronic liver disease (CLD)) ranges from 60-80 % and mortality from bleeding between 17 and 57 %. In 1996 the American Asso¬ciation VE advised screening in all patients with CLD. Numerous studies have attempted to find clinical, laboratory or images predictors of the presence of VE to streamline and make endoscopic screening cost effective. OBJECTIVE: Quantify and compare the predictive ability of different variables of VE : cli-nical (functional Class liver — FCL - Child-Pugh)), laboratory (platelet count)), ultrasound (spleen size and bipolar portal vein diameter)) mixed (ratio platelets / Spleen Gianini proposal)).http://revista.webs.fcm.unc.edu.arFil: Gandini, Bernardo José. Universidad Nacional de Córdoba. Facultad de Ciencias Médicas. Hospital Nacional de Clínicas. Cátedra de Clínica Médica; Argentina.Fil: Soria, Fernando. Universidad Nacional de Córdoba. Facultad de Ciencias Médicas. Hospital Nacional de Clínicas; Argentina.Fil: Werner, Marina. Universidad Nacional de Córdoba. Facultad de Ciencias Médicas. Hospital Nacional de Clínicas. Cátedra de Clínica Médica; Argentina.Fil: Benítez Eduardo. Universidad Nacional de Córdoba. Facultad de Ciencias Médicas. Hospital Nacional de Clínicas. Cátedra de Clínica Médica; Argentina.Fil: Benítez, Marta. Universidad Nacional de Córdoba. Facultad de Ciencias Médicas. Instituto de Virología "Dr. José María Vanella"; Argentina.Fil: García Oro, Agustina.Universidad Nacional de Córdoba. Facultad de Ciencias Médicas. Hospital Nacional de Clínicas; Argentina.Fil: Días, L. Universidad Nacional de Córdoba. Facultad de Ciencias Médicas. Hospital Nacional de Clínicas; Argentina.Fil: Martínez, ML. Universidad Nacional de Córdoba. Facultad de Ciencias Médicas. Hospital Nacional de Clínicas; Argentina.Fil: Gutierrez, R. Universidad Nacional de Córdoba. Facultad de Ciencias Médicas. Hospital Nacional de Clínicas; Argentina.Fil: Periolo, A. Universidad Nacional de Córdoba. Facultad de Ciencias Médicas. Hospital Nacional de Clínicas; Argentina.Fil: Salas, F. Universidad Nacional de Córdoba. Facultad de Ciencias Médicas. Hospital Nacional de Clínicas; Argentina

Decreased expression of surfactant Protein-C and CD74 in alveolar epithelial cells during influenza virus A(H1N1)pdm09 and H3N2 infection

The primary replication site of Influenza A virus (IAV) is type II alveolar epithelial cells (AECII), which are central to normal lung function and present important immune functions. Surfactant components are synthesized primarily by AECII, which play a crucial role in host defense against infection. The aim of this study was to analyze if the impact of influenza infection is differential between A(H1N1)pdm09 and A/Victoria/3/75 (H3N2) on costimulatory molecules and ProSP-C expression in AECII from BALB/c mice infected and A549 cell line infected with both strains. Pandemic A(H1N1)pdm09 and A/Victoria/3/75 (H3N2) were used to infect BALB/c mice and the A549 cell line. We evaluated the surface expression of co-stimulatory molecules (CD45/CD31/CD74/ProSP-C) in AECII and A549 cell lines. Our results showed a significant decrease in ProSP-C+ CD31− CD45– and CD74+ CD31− CD45− expression in AECII and A549 cell line with the virus strain A(H1N1)pdm09 versus A/Victoria/3/75 (H3N2) and controls (non-infection conditions). Our findings indicate that changes in the expression of ProSP-C in AECII and A549 cell lines in infection conditions could result in dysfunction leading to decreased lung compliance, increased work of breathing and increased susceptibility to injury.Fil: Ibañez, Lorena Itatí. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Ciencia y Tecnología "Dr. César Milstein". Fundación Pablo Cassará. Instituto de Ciencia y Tecnología "Dr. César Milstein"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química, Física de los Materiales, Medioambiente y Energía. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química, Física de los Materiales, Medioambiente y Energía; ArgentinaFil: Martínez, Valeria P.. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud "Dr. C. G. Malbrán"; ArgentinaFil: Iglesias, Ayelén A.. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud "Dr. C. G. Malbrán"; ArgentinaFil: Bellomo, Carla María. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud "Dr. C. G. Malbrán"; ArgentinaFil: Alonso, Daniel Oscar. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud "Dr. C. G. Malbrán"; ArgentinaFil: Coelho, Rocío María. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud "Dr. C. G. Malbrán"; ArgentinaFil: Martinez Peralta, Liliana A.. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología. Cátedra de Microbiología, Parasitología e Inmunología; ArgentinaFil: Periolo, Natalia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud "Dr. C. G. Malbrán"; Argentin

Influenza virus surveillance in Argentina during the 2012 season: antigenic characterization, genetic analysis and antiviral susceptibility

Fil: Benedetti, Estefanía. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Departamento de Virología. Servicio de Virosis Respiratoria; Argentina.Fil: Daniels, Rodney S. The Francis Crick Institute. Mill Hill Laboratory, The Ridgeway, Mill Hill, Londres; Reino Unido.Fil: Pontoriero, Andrea. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Departamento de Virología. Servicio de Virosis Respiratoria; Argentina.Fil: Russo, Mara. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Departamento de Virología. Servicio de Virosis Respiratoria; Argentina.Fil: Avaro, Martín. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Departamento de Virología. Servicio de Virosis Respiratoria; Argentina.Fil: Czech, A. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Departamento de Virología. Servicio de Virosis Respiratoria; Argentina.Fil: Campos, Ana. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Departamento de Virología. Servicio de Virosis Respiratoria; Argentina.Fil: Periolo, Natalia. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Departamento de Virología. Servicio de Virosis Respiratoria; Argentina.Fil: Gregory, V. The Francis Crick Institute. Mill Hill Laboratory, The Ridgeway, Mill Hill, Londres; Reino Unido.Fil: McCauley, John W. The Francis Crick Institute. Mill Hill Laboratory, The Ridgeway, Mill Hill, Londres; Reino Unido.Fil: Baumeister, Elsa G. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Departamento de Virología. Servicio de Virosis Respiratoria; Argentina.The activity and circulation of influenza viruses in Argentina was studied during 2012 as part of the Argentinean Surveillance for Influenza and other Respiratory Viruses, in the context of Global Influenza Surveillance. The antigenicity and molecular characteristics of haemagglutinins (HA) of circulating influenza A and B viruses were analysed to assess the emergence of virus variants. Susceptibility to oseltamivir and zanamivir was evaluated by enzymatic assay and results were backed-up by sequencing of the neuraminidase (NA) genes. During the 2012 season, influenza virus circulation in Argentina was detected from weeks 24 to 51. The HA sequences of the studied A(H1N1)pdm09 subtype viruses segregated in a different genetic group compared to those identified during the 2009 pandemic, although they were still closely related antigenically to the vaccine virus A/California/07/2009. The HA sequences of the A(H3N2) viruses analysed fell into the A/Victoria/208/2009 clade, genetic group 3C. A mixed circulation of virus variants belonging to B/Victoria and B/Yamagata lineages was detected, with B/Victoria being dominant. All viruses tested were sensitive to oseltamivir and zanamivir except one. This isolate, an A(H1N1)pdm09 virus possessing the substitution NA-N295S, showed highly reduced inhibition by oseltamivir and reduced inhibition by zanamivir. Virological and epidemiological surveillance remains critical for detection of evolving influenza viruses

Altered expression of the lymphocyte activation antigen CD30 in active celiac disease

Interleukin (IL)-15 and CD30 may be associated with the ongoing intestinal immunologic activation in celiac disease (CD). We studied duodenal biopsies and blood samples of patients with active CD (Cel) and controls in order to determine the regulatory role proposed for CD30þ T cells in this Th1-driven disease and the potential influences of IL-15 on CD30 expression. We detected that a CD30þ T-cell subpopulation persists longer in Cel after a 5 day incubation with anti-CD3 antibody than in controls ( p ¼ 0.0063). CD30 upregulation by IL-15 in T blasts was greater in Cel than in controls ( p ¼ 0.0062). At the mucosal compartment, the CD30 antigen was examined by immunohistochemistry and quantified on isolated lamina propria (LP) and epithelial T cells by flow cytometry. For Cel and controls, similar mean percentages of CD3þCD30þ intraepithelial T cells (5.88 vs. 5.51, p ¼ ns) and LP T cells (7.38 vs. 7.49, p ¼ ns) were observed at baseline and after in vitro gliadin challenge of duodenal biopsy samples. Our study demonstrates the occurrence of potentially important alterations of the immune response at the peripheral compartment. Our findings also allow us to speculate that a negative effect of soluble mediators at the mucosal compartment might counteract the latent influence of IL-15 on CD30 expression precluding a more severe course of active CD.Fil: Periolo, Natalia. Direccion Nacional de Instituto de Investigacion. Administración Nacional de Laboratorio e Instituto de Salud "Dr. C. G. Malbran". Instituto Nacional de Enfermedades Infecciosas. Departamento de Virologia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFil: Guillen, Laura Cristina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFil: Bernardo, D.. Universidad de Valladolid. Facultad de Ciencias; EspañaFil: Niveloni, Sonia Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFil: Hwang, H. J.. Gobierno de la Ciudad de Buenos Aires. Hospital de Gastroenterología "Dr. Carlos B. Udaondo"; ArgentinaFil: Garrote, J. A.. Gobierno de la Ciudad de Buenos Aires. Hospital de Gastroenterología "Dr. Carlos B. Udaondo"; Argentina. Hospital Clínico Universitario; EspañaFil: BaI, J. C.. Gobierno de la Ciudad de Buenos Aires. Hospital de Gastroenterología "Dr. Carlos B. Udaondo"; ArgentinaFil: Arranz, Silvia Eda. Universidad de Valladolid. Facultad de Ciencias; EspañaFil: Cherñavsky, Alejandra Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentin

Liver infiltrating mononuclear cells in children with type 1 autoimmune hepatitis

OBJECTIVE: To investigate infiltrating cells in the liver of children with type 1 autoimmune hepatitis (AH‐1). METHODS: liver biopsies from 24 untreated AH‐1 patients (14 children, 10 adults), five patients with hepatitis C virus related chronic hepatitis (HCV), and 10 control liver specimens (CL) were processed for immunohistochemical cell characterisation. RESULTS: Two different cell distribution patterns were detected in the liver of patients with AH‐1: (1) CD4(+) and CD20(+) cells were found in the central areas of the portal tracts (portal distribution); (2) CD8(+) cells were observed at the periphery of the portal space (periportal distribution). Some cell subsets, like CD56, CD57, Fas‐L, and Bak, showed a non‐defined distribution pattern. The presence of two well defined patterns of cell distribution was not observed in HCV and CL (CD4(+), CD20(+), and CD8(+) cells were uniformly distributed in the portal space). In AH‐1 and CL, the NK markers CD56 and CD57 were found scattered throughout the liver parenchyma. However, in HCV biopsies, CD56(+) cells were also clearly increased in both the portal and the periportal areas. Biopsies of AH‐1 and HCV patients showed a uniform distribution of Fas‐L and Bak in the portal and periportal areas, with Bak staining also detected in the hepatic parenchyma. CONCLUSIONS: Despite clinical and genetic differences, there was a similar distribution of liver infiltrating mononuclear cells in children and adults with AH‐1. These results raise the possibility of reclassifying cryptogenic chronic hepatitis by immunohistochemical analysis of infiltrating liver cells

Impact of Toll-Like Receptor 2 Deficiency on Immune Responses to Mycobacterial Antigens▿ †

In the present study, we addressed the question of whether Toll-like receptor 2 (TLR2)-mediated innate immunity can contribute to the development of acquired immune responses. We immunized TLR2−/− and wild-type (WT) mice three times subcutaneously with the mycobacterial antigen (Ag19kDa) (a TLR2 ligand) or Ag85A (not a TLR2 ligand). One week after the last immunization, sera and spleens were collected. To evaluate cellular responses, we measured gamma interferon (IFN-γ) after in vitro restimulation of spleen cells with antigen alone or antigen-pulsed bone marrow-derived macrophages (BMMAg) or pulmonary macrophages (PuMAg). Antibody responses were comparable in the two mouse strains, but we observed differences in the cellular responses. Recall responses to Ag85A were similar in the two strains, but responses to Ag19kDa given alone or presented by BMM or PuM were lower in TLR2−/− than in WT mice. The largest differences in cellular responses were observed when Ag19kDa was presented by PuM. To understand this, we analyzed phenotypic and functional differences between BMM and PuM upon stimulation with various ligands. Generally, PuM had a lower response to the TLR2 ligand Pam3Cys-Ser-(Lys)4 trihydrochloride and to anti-CD40 than BMM, as measured by cytokine secretion and upregulation of costimulatory molecules. This might provide a partial explanation for the lower capacity of PuM when pulsed with Ag19kDa, also a TLR2 ligand. Altogether, our results revealed weaknesses in the T cell and antigen-presenting cell (APC) compartments of the Ag19kDa-immunized TLR2−/− mice but indicated that specific immune responses could be generated in the absence of TLR2 regardless of the characteristics of the antigen used