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Browsing by Author "Riedel, Claudia A."

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Aldosterone Promotes Autoimmune Damage by Enhancing Th17-Mediated Immunity
(AMER ASSOC IMMUNOLOGISTS, 2010) Herrada, Andres A.; Contreras, Francisco J.; Marini, Natacha P.; Amador, Cristian A.; Gonzalez, Pablo A.; Cortes, Claudia M.; Riedel, Claudia A.; Carvajal, Cristian A.; Figueroa, Fernando; Michea, Luis F.; Fardella, Carlos E.; Kalergis, Alexis M.
Excessive production of aldosterone leads to the development of hypertension and cardiovascular disease by generating an inflammatory state that can be promoted by T cell immunity. Because nature and intensity of T cell responses is controlled by dendritic cells (DCs), it is important to evaluate whether the function of these cells can be modulated by aldosterone. In this study we show that aldosterone augmented the activation of CD8(+) T cells in a DC-dependent fashion. Consistently, the mineralocorticoid receptor was expressed by DCs, which showed activation of MAPK pathway and secreted IL-6 and TGF-beta in response to aldosterone. In addition, DCs stimulated with aldosterone impose a Th17 phenotype to CD4(+) T cells, which have recently been associated with the promotion of inflammatory and autoimmune diseases. Accordingly, we observed that aldosterone enhances the progression of experimental autoimmune encephalomyelitis, an autoimmune disease promoted by Th17 cells. In addition, blockade of the mineralocorticoid receptor prevented all aldosterone effects on DCs and attenuated experimental autoimmune encephalomyelitis development in aldosterone-treated mice. Our data suggest that modulation of DC function by aldosterone enhances CD8(+) T cell activation and promotes Th17-polarized immune responses, which might contribute to the inflammatory damage leading to hypertension and cardiovascular disease. The Journal of Immunology, 2010, 184: 191-202.
Altered Chemokine Receptor Expression in Papillary Thyroid Cancer
(MARY ANN LIEBERT, INC, 2009) Gonzalez, Hernan E.; Leiva, Andrea; Tobar, Hugo; Boehmwald, Karen; Tapia, Grace; Torres, Javiera; Mosso, Lorena M.; Bueno, Susan M.; Gonzalez, Pablo; Kalergis, Alexis M.; Riedel, Claudia A.
Background: Papillary thyroid cancer (PTC), the most prevalent type of differentiated thyroid carcinoma, displays a strikingly high frequency of lymph node metastasis (LNM). Recent data suggest that chemokines can play an important role in promoting tumor progression and metastatic migration of tumor cells. Here we have evaluated whether PTC tissues express a different pattern of chemokine receptors and if the expression of these receptors correlates with LNM.
Assessing the Importance of Domestic Vaccine Manufacturing Centers: An Overview of Immunization Programs, Vaccine Manufacture, and Distribution
(2018) Rey-Jurado, Emma; Tapia, Felipe; Munoz-Durango, Natalia; Lay, Margarita K.; Carreno, Leandro J.; Riedel, Claudia A.; Bueno Ramírez, Susan; Genzel, Yvonne; Kalergis Parra, Alexis Mikes
Asymptomatic herpes simplex virus brain infection elicits cellular senescence phenotypes in the central nervous system of mice suffering multiple sclerosis-like disease
(2024) Duarte, Luisa F.; Villalobos, Veronica; Farias, Monica A.; Rangel-Ramirez, Ma. Andreina; Gonzalez-Madrid, Enrique; Navarro, Areli J.; Carbone-Schellman, Javier; Dominguez, Angelica; Alvarez, Alejandra; Riedel, Claudia A.; Bueno, Susan M.; Kalergis, Alexis M.; Caceres, Monica; Gonzalez, Pablo A.
Experimental autoimmune encephalomyelitis (EAE) is a demyelinating disease affecting the central nervous system (CNS) in animals that parallels several clinical and molecular traits of multiple sclerosis in humans. Herpes simplex virus type 1 (HSV-1) infection mainly causes cold sores and eye diseases, yet eventually, it can also reach the CNS, leading to acute encephalitis. Notably, a significant proportion of healthy individuals are likely to have asymptomatic HSV-1 brain infection with chronic brain inflammation due to persistent latent infection in neurons. Because cellular senescence is suggested as a potential factor contributing to the development of various neurodegenerative disorders, including multiple sclerosis, and viral infections may induce a premature senescence state in the CNS, potentially increasing susceptibility to such disorders, here we examine the presence of senescence-related markers in the brains and spinal cords of mice with asymptomatic HSV-1 brain infection, EAE, and both conditions. Across all scenarios, we find a significant increases of senescence biomarkers in the CNS with some differences depending on the analyzed group. Notably, some senescence biomarkers are exclusively observed in mice with the combined conditions. These results indicate that asymptomatic HSV-1 brain infection and EAE associate with a significant expression of senescence biomarkers in the CNS.
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.
Circulating Endothelial Cells From Septic Shock Patients Convert to Fibroblasts Are Associated With the Resuscitation Fluid Dose and Are Biomarkers for Survival Prediction.
(2019) Tapia, Pablo; Gatica, Sebastian; Cortés-Rivera, Cristian; Otero, Carolina; Becerra, Álvaro; Riedel, Claudia A.; Cabello-Verrugio, Claudio; Kalergis, Alexis M.; Simon, Felipe
OBJECTIVES:To determine whether circulating endothelial cells from septic shock patients and from nonseptic shock patients are transformed in activated fibroblast by changing the expression level of endothelial and fibrotic proteins, whether the level of the protein expression change is associated with the amount of administered resuscitation fluid, and whether this circulating endothelial cell protein expression change is a biomarker to predict sepsis survival. DESIGN:Prospective study. SETTING:Medical-surgical ICUs in a tertiary care hospital. PATIENTS:Forty-three patients admitted in ICU and 22 healthy volunteers. INTERVENTIONS:None. MEASUREMENTS AND MAIN RESULTS:Circulating mature endothelial cells and circulating endothelial progenitor cells from septic shock and nonseptic shock patients showed evidence of endothelial fibrosis by changing the endothelial protein expression pattern. The endothelial proteins were downregulated, whereas fibroblast-specific markers were increased. The magnitude of the expression change in endothelial and fibrotic proteins was higher in the septic shock nonsurvivors patients but not in nonseptic shock. Interestingly, the decrease in the endothelial protein expression was correlated with the administered resuscitation fluid better than the Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores in the septic shock nonsurvivors patients but not in nonseptic shock. Notably, the significant difference between endothelial and fibrotic protein expression indicated a nonsurvival outcome in septic shock but not in nonseptic shock patients. Remarkably, area under the receiver operating characteristic curve analysis showed that endothelial protein expression levels predicted the survival outcome better than the Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores in septic shock but not in nonseptic shock patients. CONCLUSIONS:Circulating endothelial cells from septic shock patients are acutely converted into fibroblasts. Endothelial and fibrotic protein expression level are associated with resuscitation fluid administration magnitude and can be used as biomarkers for an early survival diagnosis of sepsis.
Contribution of autophagy to antiviral immunity
(2015) Rey-Jurado, Emma; Riedel, Claudia A.; Gonzalez, Pablo A.; Bueno Ramírez, Susan; Kalergis Parra, Alexis Mikes
Contribution of dendritic cells to the autoimmune pathology of systemic lupus erythematosus
(2015) Mackern Oberti, Juan Pablo; Llanos Muñoz, Carolina; Riedel, Claudia A.; Bueno Ramírez, Susan; Kalergis Parra, Alexis Mikes
Deletion of a prophage-like element causes attenuation of Salmonella enterica serovar Enteritidis and promotes protective immunity
(2010) Araya, Daniela V.; Quiroz, Tania S.; Tobar, Hugo E.; Lizana, Rodrigo J.; Quezada, Carolina P.; Santiviago, Carlos A.; Riedel, Claudia A.; Kalergis, Alexis M.; Bueno, Susan M.
Salmonella enterica serovar Enteritidis (S Enteritidis) is a wide host range serovar belonging to the S. enterica genus. Worldwide, it is one of the most frequent causes of food borne disease Similar to S. Typhimurium, some virulence genes of S. Enteritidis are located in pathogenicity islands and prophages. In this study we have generated a mutant strain of S. Enteritidis lacking a prophage-like element, denominated phi SE12. The resulting mutant strain was attenuated and promoted protective immunity in infected mice Although S Enteritidis strains lacking the complete prophage phi SE12 remained capable of surviving inside phagocytic cells, they showed a significantly reduced capacity to colonize internal organs and failed to cause lethal disease in mice. Consistent with these data, infection with S Enteritidis strains lacking prophage phi SE12 promoted the production of anti-Salmonella IgG antibodies and led to protection against a challenge with virulent strains of S Enteritidis. These results suggest that strains lacking this prophage can induce a protective immunity in mice and be considered as potential attenuated vaccines against S Enteritidis. (C) 2010 Elsevier Ltd All rights reserved
Differential Severe Acute Respiratory Syndrome Coronavirus 2-Specific Humoral Response in Inactivated Virus-Vaccinated, Convalescent, and Breakthrough-Infected Subjects
(OXFORD UNIV PRESS INC, 2023) Duarte Peñaloza, Luisa Fernanda; Vazquez Hernandez Yaneisi; Diethelm Varela, Benjamin Manuel; Pavez, Valentina; Berrios-Rojas, Roslye; Riedel, Claudia A.; Mendez, Constanza; White, Jessica A.; Kalergis Parra, Alexis Mikes; Bueno Ramírez, Susan Marcela; González Muñoz, Pablo Alberto
Background. We sought to identify potential antigens for discerning between humoral responses elicited after vaccination with CoronaVac (a severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2] inactivated vaccine), natural infection, or breakthrough infection., Methods. Serum samples obtained from volunteers immunized with CoronaVac (2 and 3 doses), breakthrough case patients, and from convalescent individuals were analyzed to determine the immunoglobulin (Ig) G responses against 3 structural and 8 nonstructural SARS-CoV-2 antigens., Results. Immunization with CoronaVac induced higher levels of antibodies against the viral membrane (M) protein compared with convalescent subjects both after primary vaccination and after a booster dose. Individuals receiving a booster dose displayed equivalent levels of IgG antibodies against the nucleocapsid (N) protein, similar to convalescent subjects. Breakthrough case patients produced the highest antibody levels against the N and M proteins. Antibodies against nonstructural viral proteins were present in >50% of the convalescent subjects., Conclusions. Vaccinated individuals elicited a different humoral response compared to convalescent subjects. The analysis of particular SARS-CoV-2 antigens could be used as biomarkers for determining infection in subjects previously vaccinated with CoronaVac.
Efficient Lung Recruitment of Respiratory Syncytial Virus-Specific Th1 Cells Induced by Recombinant Bacillus Calmette-Guerin Promotes Virus Clearance and Protects from Infection
(AMER ASSOC IMMUNOLOGISTS, 2010) Cautivo, Kelly M.; Bueno, Susan M.; Cortes, Claudia M.; Wozniak, Aniela; Riedel, Claudia A.; Kalergis, Alexis M.
Infection by the respiratory syncytial virus (RSV) can cause extensive inflammation and lung damage in susceptible hosts due to a Th2-biased immune response. Such a deleterious inflammatory response can be enhanced by immunization with formalin- or UV-inactivated RSV, as well as with vaccinia virus expressing the RSV-G protein. Recently, we have shown that vaccination with rBCG-expressing RSV Ags can prevent the disease in the mouse. To further understand the immunological mechanisms responsible for protection against RSV, we have characterized the T cell populations contributing to virus clearance in mice immunized with this BCG-based vaccine. We found that both CD4(+) and CD8(+) T cells were recruited significantly earlier to the lungs of infected mice that were previously vaccinated. Furthermore, we observed that simultaneous adoptive transfer of CD8(+) and CD4(+) RSV-specific T cells from vaccinated mice was required to confer protection against virus infection in naive recipients. In addition, CD4(+) T cells induced by vaccination released IFN-gamma after RSV challenge, indicating that protection is mediated by a Th1 immune response. These data suggest that vaccination with rBCG-expressing RSV Ags can induce a specific effector/memory Th1 immune response consisting on CD4(+) and CD8(+) T cells, both necessary for a fully protective response against RSV. These results support the notion that an effective induction of Th1 T cell immunity against RSV during childhood could counteract the unbalanced Th2-like immune response triggered by the natural RSV infection. The Journal of Immunology, 2010, 185: 7633-7645.
Excision of an Unstable Pathogenicity Island in Salmonella enterica Serovar Enteritidis Is Induced during Infection of Phagocytic Cells
(PUBLIC LIBRARY SCIENCE, 2011) Quiroz, Tania S.; Nieto, Pamela A.; Tobar, Hugo E.; Salazar Echegarai, Francisco J.; Lizana, Rodrigo J.; Quezada, Carolina P.; Santiviago, Carlos A.; Araya, Daniela V.; Riedel, Claudia A.; Kalergis, Alexis M.; Bueno, Susan M.
The availability of the complete genome sequence of several Salmonella enterica serovars has revealed the presence of unstable genetic elements in these bacteria, such as pathogenicity islands and prophages. This is the case of Salmonella enterica serovar Enteritidis (S. Enteritidis), a bacterium that causes gastroenteritis in humans and systemic infection in mice. The whole genome sequence analysis for S. Enteritidis unveiled the presence of several genetic regions that are absent in other Salmonella serovars. These regions have been denominated "regions of difference'' (ROD). In this study we show that ROD21, one of such regions, behaves as an unstable pathogenicity island. We observed that ROD21 undergoes spontaneous excision by two independent recombination events, either under laboratory growth conditions or during infection of murine cells. Importantly, we also found that one type of excision occurred at higher rates when S. Enteritidis was residing inside murine phagocytic cells. These data suggest that ROD21 is an unstable pathogenicity island, whose frequency of excision depends on the environmental conditions found inside phagocytic cells.
Expanding the current knowledge about the role of interleukin-10 to major concerning bacteria
(2018) Peñaloza Cerda, Hernán F.; Noguera, Loreani; Riedel, Claudia A.; Bueno Ramírez, Susan
Female offspring gestated in hypothyroxinemia and infected with human Metapneumovirus (hMPV) suffer a more severe infection and have a higher number of activated CD8⁺ T lymphocytes
(2022) Funes, Samanta C.; Rios, Mariana; Fernandez-Fierro, Ayleen; Rivera-Perez, Daniela; Soto, Jorge A.; Valbuena, Jose R.; Altamirano-Lagos, Maria J.; Gomez-Santander, Felipe; Jara, Evelyn L.; Zoroquiain, Pablo; Roa, Juan C.; Kalergis, Alexis M.; Riedel, Claudia A.
Maternal thyroid hormones (THs) are essential for the appropriate development of the fetus and especially for the brain. Recently, some studies have shown that THs deficiency can also alter the immune system development of the progeny and their ability to mount an appropriate response against infectious agents. In this study, we evaluated whether adult mice gestated under hypothyroxinemia (Hpx) showed an altered immune response against infection with human metapneumovirus (hMPV). We observed that female mice gestated under Hpx showed higher clinical scores after seven days of hMPV infection. Besides, males gestated under Hpx have higher lung viral loads at day seven post-infection. Furthermore, the female offspring gestated in Hpx have already reduced the viral load at day seven and accordingly showed an increased proportion of activated (CD71(+) and FasL(+)) CD8(+) T cells in the lungs, which correlated with a trend for a higher histopathological clinical score. These results support that T-4 deficiency during gestation might condition the offspring differently in males and females, enhancing their ability to respond to hMPV.
Gene Elements that Regulate Streptococcus pneumoniae Virulence and Immunity Evasion
(2013) Nieto Pacheco, Pamela Andrea; Riquelme, Sebastián A.; Riedel, Claudia A.; Kalergis Parra, Alexis Mikes; Bueno Ramírez, Susan
Genetic and pharmacological modulation of dendritic cell-T cell interactions as a therapeutic strategy for systemic lupus erythematosus.
(2011) Llanos, Carolina; Carreno, Leandro J.; Gutierrez, Miguel A.; Riedel, Claudia A.; Jacobelli, Sergio H.; Kalergis, Alexis M.
Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease characterized by an excessive production of auto-antibodies against double-stranded DNA, nucleosomes, ribonucleoproteins and other nuclear components. Accumulation of self-reactive antibodies leads to immune complex deposition in blood vessels, activation of macrophages and complement, inflammation and subsequent tissue damage in several organs, such as the heart, kidneys, lungs and central nervous system. Although significant progress has been made in the past 30 years of research, no effective specific treatments are currently available. The course of this disease remains unpredictable and patients diagnosed with SLE face long-term treatments with the subsequent economic, social and health burden. From the immunological perspective, SLE is a genetic- and environment-controlled disease that involves almost every constituent of the immune system, including both innate and adaptive immunity. Therefore, several immune cell types and molecules could be susceptible for intervention and modulation to develop more effective and specific treatments. More importantly, such therapies are likely not to induce complete immunosuppression and show reduced side effects on patients. In this article we discuss recent work in the field of SLE pathogenesis with a focus on data that provide clues for therapy design and new treatments.
Gestational Hypothyroxinemia Imprints a Switch in the Capacity of Astrocytes and Microglial Cells of the Offspring to React in Inflammation
(2018) Opazo, María C.; González, Pablo A.; Flores, Betsi D.; Venegas, Luis F.; Albornoz, Eduardo A.; Cisternas, Pablo; Bohmwald Prieto, Karen; Nieto Pacheco, Pamela Andrea; Bueno Ramírez, Susan; Kalergis Parra, Alexis Mikes; Riedel, Claudia A.
Gestational hypothyroxinemia induces ASD-like phenotypes in behavior, proinflammatory markers, and glutamatergic protein expression in mouse offspring of both sexes
(2024) Gonzalez-Madrid, Enrique; Rangel-Ramirez, Ma. Andreina; Opazo, Maria C.; Mendez, Luis; Bohmwald, Karen; Bueno, Susan M.; Gonzalez, Pablo A.; Kalergis, Alexis M.; Riedel, Claudia A.
Background The prevalence of autism spectrum disorder (ASD) has significantly risen in the past three decades, prompting researchers to explore the potential contributions of environmental factors during pregnancy to ASD development. One such factor of interest is gestational hypothyroxinemia (HTX), a frequent condition in pregnancy associated with cognitive impairments in the offspring. While retrospective human studies have linked gestational HTX to autistic traits, the cellular and molecular mechanisms underlying the development of ASD-like phenotypes remain poorly understood. This study used a mouse model of gestational HTX to evaluate ASD-like phenotypes in the offspring.Methods To induce gestational HTX, pregnant mice were treated with 2-mercapto-1-methylimidazole (MMI), a thyroid hormones synthesis inhibitor, in the tap-drinking water from embryonic days (E) 10 to E14. A separate group received MMI along with a daily subcutaneous injection of T4, while the control group received regular tap water during the entire pregnancy. Female and male offspring underwent assessments for repetitive, anxious, and social behaviors from postnatal day (P) 55 to P64. On P65, mice were euthanized for the evaluation of ASD-related inflammatory markers in blood, spleen, and specific brain regions. Additionally, the expression of glutamatergic proteins (NLGN3 and HOMER1) was analyzed in the prefrontal cortex and hippocampus.Results The HTX-offspring exhibited anxious-like behavior, a subordinate state, and impaired social interactions. Subsequently, both female and male HTX-offspring displayed elevated proinflammatory cytokines in blood, including IL-1 beta, IL-6, IL-17A, and TNF-alpha, while only males showed reduced levels of IL-10. The spleen of HTX-offspring of both sexes showed increased Th17/Treg ratio and M1-like macrophages. In the prefrontal cortex and hippocampus of male HTX-offspring, elevated levels of IL-17A and reduced IL-10 were observed, accompanied by increased expression of hippocampal NLGN3 and HOMER1. All these observations were compared to those observed in the Control-offspring. Notably, the supplementation with T4 during the MMI treatment prevents the development of the observed phenotypes. Correlation analysis revealed an association between maternal T4 levels and specific ASD-like outcomes.Discussion This study validates human observations, demonstrating for the first time that gestational HTX induces ASD-like phenotypes in the offspring, highlighting the need of monitoring thyroid function during pregnancy.
Hormonal Modulation of Dendritic Cells Differentiation, Maturation and Function: Implications for the Initiation and Progress of Systemic Autoimmunity.
(2016) Mackern-Oberti, Juan Pablo; Jara, Evelyn L.; Riedel, Claudia A.; Kalergis, Alexis M.
Hormonal homeostasis is crucial for keeping a competent and healthy immune function. Several hormones can modulate the function of various immune cells such as dendritic cells (DCs) by influencing the initiation of the immune response and the maintenance of peripheral tolerance to self-antigens. Hormones, such as estrogens, prolactin, progesterone and glucocorticoids may profoundly affect DCs differentiation, maturation and function leading to either a pro-inflammatory or an anti-inflammatory (or tolerogenic) phenotype. If not properly regulated, these processes can contribute to the pathogenesis of autoimmune disease. An unbalanced hormonal status may affect the production of pro-inflammatory cytokines, the expression of activating/inhibitory receptors and co-stimulatory molecules on conventional and plasmacytoid DCs (pDCs), conferring susceptibility to develop autoimmunity. Estrogen receptor (ER)-α signaling in conventional DCs can promote IFN-α and IL-6 production and induce the expression of CD40, CD86 and MHCII molecules. Furthermore, estrogen modulates the pDCs response to Toll-like receptor ligands enhancing T cell priming. During lupus pathogenesis, ER-α deficiency decreased the expression of MHC II on pDCs from the spleen. In contrast, estradiol administration to lupus-prone female mice increased the expression of co-stimulatory molecules, enhanced the immunogenicity and produced large amounts of IL-6, IL-12 and TNF-α by bone marrow-derived DCs. These data suggest that estradiol/ER signaling may play an active role during lupus pathology. Similarly, understanding hormonal modulation of DCs may favor the design of new therapeutic strategies based on autologous tolerogenic DCs transfer, especially in sex-biased systemic autoimmune diseases. In this review, we discuss recent data relative to the role of different hormones (estrogen, prolactin, progesterone and glucocorticoids) in DC function during systemic autoimmune pathogenesis.
Host immunity during RSV pathogenesis
(2008) Bueno Ramírez, Susan; González Muñoz, Pablo Alberto; Pacheco, Rodrigo; Leiva Llantén, Eduardo David; Cautivo Reyes, Kelly Margarita; Tobar Durán, Hugo Eduardo; Mora, Jorge E.; Prado, Carolina E.; Zuniga, Juan P.; Jimenez, Jorge; Riedel, Claudia A.; Kalergis Parra, Alexis Mikes

Browsing by Author "Riedel, Claudia A."

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