Antígenos de Helicobacter pylori en muestras fecales de usuarios con sintomatología sugestiva a gastritis que asisten a la Unidad Comunitaria de Salud Familiar Especializada de Perquin, departamento de Morazán

En la actualidad se reconoce a Helicobacter pylori como un agente patógeno involucrado en el desarrollo de gastritis crónica, úlcera gástrica y carcinoma gástrico. Lo que hace necesario realizar pruebas para detectar la presencia de la bacteria a través de diferentes métodos de laboratorio EL OBJETIVO de la investigación fué Determinar antígenos de Helicobacter pylori en muestras fecales de usuarios con sintomatología sugestiva a gastritis que asisten a la Unidad Comunitaria de Salud Familiar Especializada de Perquín, Departamento de Morazán. METODOLOGÍA de la investigación se caracterizó por ser: Prospectiva, Transversal, Descriptiva y de Laboratorio. Con una población en estudio de 97 usuarios a los cuales se les aplicó una cédula de entrevista para la recopilación de la información. A través de una muestra de heces se determinó la presencia de antígenos de Helicobacter pylori. RESULTADOS: según datos obtenidos, se determinó una positividad a la prueba de antígenos de Helicobacter pylori de 52.4% en la población femenina entre las edades de 15 a 75 años y un 38.2% en la población masculina entre las edades de 15 a 75 años. El síntoma que mayormente se presentó en la población que resultó positiva a la prueba fue dolor en la parte superior del estómago con un 87%. CONCLUSIÓN: Mediante resultados de laboratorio la presencia de antígenos de Helicobacter pylori en heces fue de 47.4% del total de la población. Comprobándose estadísticamente que la presencia de antígenos de Helicobacter pylori en las muestras fecales de usuarios con sintomatología sugestiva a gastritis es menor o igual al 40%.

Detección de antígenos de Helicobacter pylori por el método de prueba rápida en estudiantes de Bachillerato Técnico Vocacional Atención Primaria en Salud del Instituto Nacional de Usulután, municipio y departamento de Usulután

Helicobacter pylori es una bacteria gram negativa capaz de sobrevivir a la acidez gástrica provocando gastritis crónica, úlcera péptica y cáncer gástrico; las técnicas empleadas para la detección de esta bacteria se dividen en invasivas y no invasivas que brindan un diagnóstico confiable a la población en estudio. OBJETIVO: Detectar la presencia de antígenos de Helicobacter pylori por el método de prueba rápida inmunocromatográfica en heces en los estudiantes de Bachillerato Técnico Vocacional Atención Primaria en Salud del Instituto Nacional de Usulután. METODOLOGÍA: El estudio fue: prospectivo, transversal, descriptivo y de laboratorio; la información de la población en estudio se dio a conocer por medio de una cédula de entrevista; la población en estudio estuvo conformada por 167 alumnos que cursan Bachillerato Técnico Vocacional Atención Primaria en Salud del Instituto Nacional de Usulután tanto en jóvenes que presentaron sintomatología como los que no la presentaron, se le tomó una muestra de heces para la detección de antígenos de Helicobacter pylori. RESULTADO: 66 estudiantes de Bachillerato Técnico Vocacional Atención Primaria en Salud del Instituto Nacional de Usulután presentaron pruebas positivas a antígenos de Helicobacter pylori en muestras fecales y 101 resultaron negativos a la prueba. CONCLUSIÓN: la positividad a antígenos de Helicobacter pylory 39.5%, el síntoma más frecuente en los estudiantes fue reflujo gástrico con 63.2%.

Antígenos de Helicobacter pylori en muestras fecales de personas con sintomatología de reflujo gástrico que consultan en la Unidad Comunitaria de Salud Familiar Moncagua, departamento de San Miguel y Hospital Nacional San Pedro, departamento de Usulután

La bacteria Helicobacter pylori es reconocida como el principal agente causal de la gastritis crónica activa, úlcera péptica, reflujo gástrico así como un factor de predisposición del carcinoma gástrico. La detección oportuna de ésta favorece un tratamiento adecuado y evita posibles complicaciones. El Objetivo de la investigación es determinar antígenos de Helicobacter pylori en muestras fecales de personas con sintomatología de reflujo gástrico que consultan en la Unidad Comunitaria de Salud Familiar Moncagua, Departamento de San Miguel y Hospital Nacional San Pedro, Departamento de Usulután. Metodología: El estudio es de tipo prospectivo, transversal, descriptivo y de laboratorio. La población fue de 150 personas y la muestra fue de 133 personas para el Hospital Nacional San Pedro y 17 personas para la Unidad de Salud Moncagua, se realizó prueba cualitativa de antígenos de Helicobacter pylori en muestras fecales, además se administró a las personas una cédula de entrevista con la que se obtuvo información relacionada con el tema. Resultados: De 103 con reflujo gástrico en el Hospital San Pedro de Usulután 50 personas (48.5%) dieron positivos a la prueba de antígenos de Helicobacter pylori en muestras fecales y de 13 personas con este síntoma en la Unidad de Salud Moncagua de San Miguel 2 personas (15.4%) dieron positivos a la prueba. Conclusiones: El 44.8% de las personas que presentan reflujo gástrico resultaron con prueba positiva a antígenos de Helicobacter pylori en muestras fecales, por lo que se recomienda que toda persona que presenta síntoma de reflujo gástrico se realice la prueba de antígenos de Helicobacter pylori para descartar una posible infección por esta bacteria.

Caracterização Hematológica e Imunofenotípica em Pacientes com Leucemia Linfoblástica Aguda

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior

Avaliação de antígenos recombinantes de Corynebacterium pseudotuberculosis em teste sorológico para linfadenite caseosa em caprinos e ovinos

2015

Avaliação de antígenos recombinantes de Corynebacterium pseudotuberculosis em teste sorológico para linfadenite caseosa em caprinos e ovinos

2015

Cytokine synthesis by intestinal intraepithelial lymphocytes. Both gamma/delta T cell receptor-positive and alpha/beta T cell receptor-positive T cells in the G1 phase of cell cycle produce IFN-gamma and IL-5

Murine intestinal intraepithelial lymphocytes (IEL) have been shown to contain subsets of alpha/beta TCR+ and gamma/delta TCR+ T cells that spontaneously produce cytokines such as IFN-gamma and IL-5. We have now determined the nature and cell cycle stage of these cytokine-producing T lymphocytes in EIL by using IFN-gamma- and IL-5-specific ELISPOT assay, cytokine-specific mRNA-cDNA dot-blot hybridization and polymerase chain reaction, and flow cytometry (FACS) for DNA analysis. When CD3+ T cells from IEL of normal C3H/HeN mice were separated into low and high density fractions by discontinuous Percoll gradients, IFN-gamma and IL-5 spot-forming cells were only found in the former population. Analysis of mRNA for these cytokines by both IFN-gamma- and IL-5-specific dot-blot hybridization and polymerase chain reaction revealed that higher levels of message for IFN-gamma and IL-5 were also seen in the low density fraction. However, cell cycle analysis of these two fractions by FACS using propidium iodide showed a similar pattern of cell cycle stages in both low and high density populations (G0 + G1 approximately 96 to 98% and S/G2 + M approximately 2 to 4%). Finally, mRNA from gamma/delta TCR+ and alpha/beta TCR+ T cells in both low and high density fractions of IEL were analyzed for IFN-gamma and IL-5 message by polymerase chain reaction. After 35 cycles of amplification, both gamma/delta TCR+ and alpha/beta TCR+ T cells in the low density fraction expressed higher levels of message for these two cytokines when compared with the high density population. These results have now shown that both gamma/delta and alpha/beta TCR+ IEL can be separated into low and high density subsets and both fractions possess a similar stage of cell cycle. However, only the low density cells (in G1 phase) of both gamma/delta and alpha/beta TCR types possess increased cytokine-specific mRNA and produce the cytokines IFN-gamma and IL-5. Our results suggest that alpha/beta TCR+ and gamma/delta TCR+ IEL can produce cytokines without cell proliferation.

Plasma zinc and immune markers in runners in response to a moderate increase in training volume

Changes in plasma zinc concentration and markers of immune function were examined in a group of 10 male runners (n = 10) following a moderate increase in training over four weeks. Seven sedentary males acted as controls. Fasting blood samples were taken at rest, before (T0) and after (T4) four weeks of increased (+ 16 %) training and after two weeks of reduced (-31 %) training (T6). Blood was analysed for plasma zinc concentration, differential leucocyte counts, lymphocyte subpopulations and lymphocyte proliferation using incorporation of 3H-thymidine. The runners increased their training volume by 16 % over the four weeks. When compared with the nonathletes, the runners had lower concentrations of plasma zinc (p = 0.012), CD3 + (p = 0.042) and CD19 + lymphocytes (p = 0.010) over the four weeks. Lymphocyte proliferation in response to Concanavalin A stimulation was greater in the runners (p = 0.0090). Plasma zinc concentration and immune markers remained constant during the study. Plasma zinc concentration correlated with total leucocyte counts in the athletes at T6 (r = -0.72, p < 0.05) and with Pokeweed mitogen stimulation in the nonathletes at T6 (r = -0.92, p < 0.05). Therefore, athletes are unlikely to benefit from zinc supplementation during periods of moderately increased training volume.

Galectin-1 : a link between tumor hypoxia and tumor immune privilege

Purpose: To identify a 15-KDa novel hypoxia-induced secreted protein in head and neck squamous cell carcinomas (HNSCC) and to determine its role in malignant progression. Methods: We used surface-enhanced laser desorption ionization time-of-flight mass spectrometry (SELDI-TOF-MS) and tandem MS to identify a novel hypoxia-induced secreted protein in FaDu cells. We used immunoblots, real-time polymerase chain reaction (PCR), and enzyme-linked immunoabsorbent assay to confirm the hypoxic induction of this secreted protein as galectin-1 in cell lines and xenografts. We stained tumor tissues from 101 HNSCC patients for galectin-1, CA IX (carbonic anhydrase IX, a hypoxia marker) and CDS (a T-cell marker). Expression of these markers was correlated to each other and to treatment outcomes. Results: SELDI-TOF studies yielded a hypoxia-induced peak at 15 kDa that proved to be galectin-1 by MS analysis. Immunoblots and PCR studies confirmed increased galectin-1 expression by hypoxia in several cancer cell lines. Plasma levels of galectin-1 were higher in tumor-bearing severe combined immunodeficiency (SCID) mice breathing 10% O 2 compared with mice breathing room air. In HNSCC patients, there was a significant correlation between galectin-1 and CA IX staining (P = .01) and a strong inverse correlation between galectin-1 and CDS staining (P = .01). Expression of galectin-1 and CDS were significant predictors for overall survival on multivariate analysis. Conclusion: Galectin-1 is a novel hypoxia-regulated protein and a prognostic marker in HNSCC. This study presents a new mechanism on how hypoxia can affect the malignant progression and therapeutic response of solid tumors by regulating the secretion of proteins that modulate immune privilege. © 2005 by American Society of Clinical Oncology.

Ultraviolet Photodissociation of the N-Methylpyridinium Ion: Action Spectroscopy and Product Characterization

The ultraviolet photodissociation of gas-phase N-methylpyridinium ions is studied at room temperature using laser photodissociation mass spectrometry and structurally diagnostic ion-molecule reaction kinetics. The C5H5N-CH3+ (m/z 94), C5H5N-CD3+ (m/z 97), and C5D5N-CH3+(m/z 99) isotopologues are investigated, and it is shown that the N-methylpyridinium ion photodissociates by the loss of methane in the 36 000 - 43 000 cm(-1) (280 - 230 nm) region. The dissociation likely occurs on the ground state surface following internal conversion from the SI state. For each isotopologue, by monitoring the photofragmentation yield as a function of photon wavenumber, a broad vibronically featured band is recorded with origin (0-0) transitions assigned at 38 130, 38 140 and 38 320 cm(-1) for C5H5N-CH3+ C5H5N-CD3+ and C5D5N-CH3+, respectively. With the aid of quantum chemical calculations (CASSCF(6,6)/aug-cc-pVDZ), most of the observed vibronic detail is assigned to two in-plane ring deformation modes. Finally, using ion-molecule reactions, the methane coproduct at m/z 78 is confirmed as a 2-pyridinylium ion.

Antibody-based immunotherapy for ovarian cancer: where are we at?

Cytoreductive surgery and chemotherapy continue to be the mainstay of ovarian cancer treatment. However, as mortality from advanced ovarian cancer remains very high, novel therapies are required to be integrated into existing treatment regimens. Immunotherapy represents an alternative and rational therapeutic approach for ovarian cancer based on a body of evidence supporting a protective role of the immune system against these cancers, and on the clinical success of immunotherapy in other malignancies. Whether or not immunotherapy will have a role in the future management of ovarian cancer is too early to tell, but research in this field is active. This review will discuss recent clinical developments of selected immunotherapies for ovarian cancer which fulfil the following criteria: (i) they are antibody-based, (ii) target a distinct immunological pathway, and (iii) have reached the clinical trial stage. Specifically, the focus is on Catumaxomab (anti-EpCAM × anti-CD3), Abagovomab, Oregovomab (anti-CA125), Daclizumab (anti-CD25), Ipilimumab (anti-CTLA-4), and MXD-1105 (anti-PD-L1). Catumaxomab has reached phase III clinical trials and exhibits promise with reports, showing that it can cause a significant and sustained reduction in ascites. Phase I–III clinical trials continue to be conducted on the other antibodies, some of which have had encouraging reports. We will also provide our perspective on the future of immunotherapy for ovarian cancer, and how it may be best employed in treatment regimens.

Enrichment of circulating interleukin-17-secreting interleukin-23 receptor-positive γ/δ T cells in patients with active ankylosing spondylitis

Objective Ankylosing spondylitis (AS) is a common inflammatory arthritis affecting primarily the axial skeleton. IL23R is genetically associated with AS. This study was undertaken to investigate and characterize the role of interleukin-23 (IL-23) signaling in AS pathogenesis. Methods The study population consisted of patients with active AS (n = 17), patients with psoriatic arthritis (n = 8), patients with rheumatoid arthritis, (n = 9), and healthy subjects (n = 20). IL-23 receptor (IL-23R) expression in T cells was determined in each subject group, and expression levels were compared. Results The proportion of IL-23R-expressing T cells in the periphery was 2-fold higher in AS patients than in healthy controls, specifically driven by a 3-fold increase in IL-23R-positive γ/δ T cells in AS patients. The proportions of CD4+ and CD8+ cells that were positive for IL-17 were unchanged. This increased IL-23R expression on γ/δ T cells was also associated with enhanced IL-17 secretion, with no observable IL-17 production from IL-23R-negative γ/δ T cells in AS patients. Furthermore, γ/δ T cells from AS patients were heavily skewed toward IL-17 production in response to stimulation with IL-23 and/or anti-CD3/CD28. Conclusion Recently, mouse models have shown IL-17-secreting γ/δ T cells to be pathogenic in infection and autoimmunity. Our data provide the first description of a potentially pathogenic role of these cells in a human autoimmune disease. Since IL-23 is a maturation and growth factor for IL-17-producing cells, increased IL-23R expression may regulate the function of this putative pathogenic γ/δ T cell population.

Interleukin-23 mediates the intestinal response to microbial β-1,3-glucan and the development of spondyloarthritis pathology in SKG mice

Objective Spondyloarthritides (SpA) occur in 1% of the population and include ankylosing spondylitis (AS) and arthropathy of inflammatory bowel disease (IBD), with characteristic spondylitis, arthritis, enthesitis, and IBD. Genetic studies implicate interleukin-23 (IL-23) receptor signaling in the development of SpA and IBD, and IL-23 overexpression in mice is sufficient for enthesitis, driven by entheseal-resident T cells. However, in genetically prone individuals, it is not clear where IL-23 is produced and how it drives the SpA syndrome, including IBD or subclinical gut inflammation of AS. Moreover, it is unclear why specific tissue involvement varies between patients with SpA. We undertook this study to determine the location of IL-23 production and its role in SpA pathogenesis in BALB/c ZAP-70W163C-mutant (SKG) mice injected intraperitoneally with β-1,3-glucan (curdlan). Methods Eight weeks after curdlan injection in wild-type or IL-17A-/- SKG or BALB/c mice, pathology was scored in tissue sections. Mice were treated with anti-IL-23 or anti-IL-22. Cytokine production and endoplasmic reticulum (ER) stress were determined in affected organs. Results In curdlan-treated SKG mice, arthritis, enthesitis, and ileitis were IL-23 dependent. Enthesitis was specifically dependent on IL-17A and IL-22. IL-23 was induced in the ileum, where it amplified ER stress, goblet cell dysfunction, and proinflammatory cytokine production. IL-17A was pathogenic, while IL-22 was protective against ileitis. IL-22+CD3- innate-like cells were increased in lamina propria mononuclear cells of ileitis-resistant BALB/c mice, which developed ileitis after curdlan injection and anti-IL-22. Conclusion In response to systemic β-1,3-glucan, intestinal IL-23 provokes local mucosal dysregulation and cytokines driving the SpA syndrome, including IL-17/IL-22-dependent enthesitis. Innate IL-22 production promotes ileal tolerance.

IgE+ B cells are scarce, but allergen-specific B cells with a memory phenotype circulate in patients with allergic rhinitis

Background Despite the critical role of immunoglobulin E (IgE) in allergy, circulating IgE+ B cells are scarce. Here, we describe in patients with allergic rhinitis B cells with a memory phenotype responding to a prototypic aeroallergen. Methods Fifteen allergic rhinitis patients with grass pollen allergy and 13 control subjects were examined. Blood mononuclear cells stained with carboxyfluorescein diacetate succinimidyl ester (CFSE) were cultured with Bahia grass pollen. Proliferation and phenotype were assessed by multicolour flow cytometry. Results In blood of allergic rhinitis patients with high serum IgE to grass pollen, most IgEhi cells were CD123+ HLA-DR- basophils, with IgE for the major pollen allergen (Pas n 1). Both B and T cells from pollen-allergic donors showed higher proliferation to grass pollen than nonallergic donors (P = 0.002, and 0.010, respectively), whereas responses to vaccine antigens and mitogen did not differ between groups. Allergen-driven B cells that divided rapidly (CD19mid CD3- CFSElo) showed higher CD27 (P = 0.008) and lower CD19 (P = 0.004) and CD20 (P = 0.004) expression than B cells that were slow to respond to allergen (CD19hi CD3- CFSEmid). Moreover, rapidly dividing allergen-driven B cells (CD19mid CFSElo CD27hi) showed higher expression of the plasmablast marker CD38 compared with B cells (CD19hi CFSEmid CD27lo) that were slow to divide. Conclusion Patients with pollen allergy but not control donors have a population of circulating allergen-specific B cells with the phenotype and functional properties of adaptive memory B-cell responses. These cells could provide precursors for allergen-specific IgE production upon allergen re-exposure. © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.