Browsing by Author "Sebastián Quijada, Valentina Pilar"

Now showing 1 - 6 of 6
  • Thumbnail Image
    Item
    A potential role of Salmonella infection in the onset of inflammatory bowel diseases
    (2017) Schultz, B.; Paduro, C.; Salazar, G.; Salazar Echegarai, F.; Sebastián Quijada, Valentina Pilar; Riedel, C.; Kalergis Parra, Alexis Mikes; Álvarez Lobos, M.; Bueno Ramírez, Susan
  • Thumbnail Image
    Item
    Characterization of the anti-inflammatory capacity of IL-10-Producing neutrophils in response to streptococcus pneumoniae infection
    (FRONTIERS MEDIA SA, 2021) González Carreño, Liliana Andrea; Melo González, Felipe Andrés; Sebastián Quijada, Valentina Pilar; Vallejos Galvez, Omar Patricio; Noguera Mijares, Loreani Paola; Suazo Galvez, Isidora del Carmen; Schultz Lombardic, Bárbara M.; Manosalva, Andres H.; Peñaloza, Hernán F.; Soto Ramírez, Jorge Andres; Parker, Dane; Riedel, Claudia A.; González Muñoz, Pablo Alberto; Kalergis Parra, Alexis Mikes; Bueno Ramírez, Susan
    Neutrophils are immune cells classically defined as pro-inflammatory effector cells. However, current accumulated evidence indicates that neutrophils have more versatile immune-modulating properties. During acute lung infection with Streptococcus pneumoniae in mice, interleukin-10 (IL-10) production is required to temper an excessive lung injury and to improve survival, yet the cellular source of IL-10 and the immunomodulatory role of neutrophils during S. pneumoniae infection remain unknown. Here we show that neutrophils are the main myeloid cells that produce IL-10 in the lungs during the first 48 h of infection. Importantly, in vitro assays with bone-marrow derived neutrophils confirmed that IL-10 can be induced by these cells by the direct recognition of pneumococcal antigens. In vivo, we identified the recruitment of two neutrophil subpopulations in the lungs following infection, which exhibited clear morphological differences and a distinctive profile of IL-10 production at 48 h post-infection. Furthermore, adoptive transfer of neutrophils from WT mice into IL-10 knockout mice (Il10(-/-) ) fully restored IL-10 production in the lungs and reduced lung histopathology. These results suggest that IL-10 production by neutrophils induced by S. pneumoniae limits lung injury and is important to mediate an effective immune response required for host survival.
  • Thumbnail Image
    Item
    Heme oxygenase 1 contribution to modulating the severity of salmonella enterica serovar typhimurium infection in mice.
    (2019) Sebastián Quijada, Valentina Pilar; Bueno Ramírez, Susan; Pontificia Universidad Católica de Chile. Facultad de Ciencias Biológicas
    Salmonella enterica es un bacilo Gramnegativo perteneciente a la clase de las Gammaproteobacterias, cuyos serovares son capaces de causar enfermedades gastrointestinales y sistémicas en animales y humanos. En particular Salmonella enterica serovar Typhimurium (S. Typhimurium) es la causa más común de intoxicación por alimentos contaminados y en ratones es capaz de causar una enfermedad sistémica, muy parecida a la fiebre tifoidea causada por Salmonella enterica serovar Typhi en humanos. Su reservorio natural comprende aves de corral y sus huevos, reptiles y otros mamíferos, y se transmite a través del consumo de alimentos o agua contaminada. Una de las principales características que hacen de Salmonella enterica serovar Typhimurium una bacteria virulenta es su habilidad de evadir el sistema inmune del hospedero, generando infecciones sistémicas y persistentes. Una de las moléculas inmunomoduladoras expresadas por las células del hospedero que juega un rol en la eliminación de bacterias es Hemoxigenasa 1. Hemoxigenasa 1 es una enzima que cataliza la degradación del grupo hemo en Fe3+, biliverdina y monóxido de carbono. El rol de la actividad de Hemoxigenasa 1 durante una infección por S. Typhimurium no está claro y estudios previos muestran resultados contradictorios. En este estudio, evaluamos el efecto de la inducción farmacológica de HMOX1 en un modelo de infección aguda y persistente por S. Typhimurium. Para abordar esto, indujimos la expresión de Hemoxigenasa 1 e inhibimos su actividad enzimática en ratones mediante el tratamiento con protoporfirina de cobalto o protoporfirina de estaño, respectivamente, antes de una infección con S. Typhimurium. Observamos que la inducción de Hemoxigenasa 1 con protoporfirina de cobalto no tiene mayor efecto en el score clínico y en la supervivencia de los ratones infectados con S. Typhimurium. Sin embargo, el tratamiento con protoporfirina de cobalto redujo la carga bacteriana en órganos 5 días post-infección, mientras que los ratones 12 tratados con protoporfirina de estaño mostraron cargas similares a las de los ratones tratados con vehículo. Además, la inducción de Hemoxigenasa 1 elimina la carga bacteriana cuando el tratamiento con protoporfirina de cobalto se realiza después de la infección en un modelo de infección persistente por S. Typhimurium, mientras que el tratamiento con protoporfirina de estaño resultó en valores de bacterias persistentes similares a los observados en ratones tratados con vehículo. Nuestros resultados sugieren que la actividad de Hemoxigenasa 1 puede promover la eliminación de S. Typhimurium, reduciendo la diseminación y la persistencia de la bacteria en ratones.
  • Thumbnail Image
    Item
    Heme oxygenase-1 as a modulator of intestinal inflammation development and progression
    (2018) Sebastián Quijada, Valentina Pilar; Salazar, Geraldyne; Coronado Arrázola, Irenice; Schultz, Bárbara; Vallejos, Omar; Berkowitz Fiebich, Loni; Álvarez Lobos, Manuel; Riedel, Claudia; Kalergis Parra, Alexis Mikes; Bueno Ramírez, Susan
  • Thumbnail Image
    Item
    Impact of cigarette smoking on the gastrointestinal tract inflammation: Opposing effects in Crohn\'s disease and ulcerative colitis
    (2018) Berkowitz Fiebich, Loni; Schultz Lombardic, Bárbara M.; Salazar Tapia, Geraldyne Alessandra; Pardo Roa, Catalina; Sebastián Quijada, Valentina Pilar; Álvarez Lobos, Manuel; Bueno Ramírez, Susan
    Cigarette smoking is a major risk factor for gastrointestinal disorders, such as peptic ulcer, Crohn's disease (CD), and several cancers. The mechanisms proposed to explain the role of smoking in these disorders include mucosal damage, changes in gut irrigation, and impaired mucosal immune response. Paradoxically, cigarette smoking is a protective factor for the development and progression of ulcerative colitis (UC). UC and CD represent the two most important conditions of inflammatory bowel diseases, and share several clinical features. The opposite effects of smoking on these two conditions have been a topic of great interest in the last 30 years, and has not yet been clarified. In this review, we summarize the most important and well-understood effects of smoking in the gastrointestinal tract; and particularly, in intestinal inflammation, discussing available studies that have addressed the causes that would explain the opposite effects of smoking in CD and UC.
  • Thumbnail Image
    Item
    The absence of interleukin 10 affects the morphology, differentiation, granule content and the production of cryptidin-4 in Paneth cells in mice.
    (2019) Berkowitz Fiebich, Loni; Pardo Roa, Catalina; Ramírez Rojas, Gigliola; Vallejos Galvez, Omar Patricio; Sebastián Quijada, Valentina Pilar; Riedel, Claudia A.; Álvarez Lobos, Manuel; Bueno Ramírez, Susan
    Paneth cells (PCs) are specialized epithelial cells of the small bowel that contain multiple secretory granules filled with antimicrobial peptides and trophic factors, which are essential for the control of the microorganisms growth and maintaining intestinal integrity. Alterations in their function are associated with an imbalance of the normal microbiota, gastrointestinal infections and inflammatory processes, such as Crohn's disease (CD). One of the most common murine models for studying CD is IL-10-/- mouse. IL-10-/- mice when housed in conventional conditions and take contact with commensal microorganisms develop an acute enterocolitis mediated by a Th1 immune response. Even though, alterations in PCs function are related to CD, they had not been characterized yet in this mouse model. Here we show that in specific pathogen free conditions IL-10-/- mice have aberrant granules and a large number of immature PCs at the bottom of the crypt in the ileum of IL-10-/- mice before developing intestinal inflammation, along with a reduced expression of Indian Hedgehog. In addition, IL-10-/- Paneth cells presented a reduced expression of cryptidin-4, and a heterogeneous distribution of lysozyme+ granules. The alterations in the maturation of the PCs at the bottom of the crypt were not modified after the colonization by the conventional microbiota. On the other hand, depletion of microbiota altered the phenotype, but did not normalize PCs. Our results suggest that IL-10 could be necessary for the integrity of PCs. Moreover, our results help to explain why IL-10-/- mice develop enterocolitis in response to microorganisms.