DSpace Angular :: Browsing by Author "Muñoz Durango, Natalia"

Browsing by Author "Muñoz Durango, Natalia"

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Aldosterona e IL-17 en la génesis de la hipertensión arterial mineralocorticoídea, un estudio ex vivo
(2016) Vecchiola Cárdenas, Andrea Paola; Cristóbal Fuentes, Z.; Muñoz Durango, Natalia; Tapia Castillo, Alejandra; González Gómez, Luis M.; Baudrand Biggs, René; Carvajal Maldonado, Cristián Andrés; Campino Johnson, María del Carmen; Kalergis Parra, Alexis Mikes; Carlos, F.; Lagos, A.; Fardella B., Carlos; Vecchiola Cárdenas, Andrea Paola; Cristóbal Fuentes, Z.; Muñoz Durango, Natalia; Tapia Castillo, Alejandra; González Gómez, Luis M.; Baudrand Biggs, René; Carvajal Maldonado, Cristián Andrés; Campino Johnson, María del Carmen; Kalergis Parra, Alexis Mikes; Carlos, F.; Lagos, A.; Fardella B., Carlos
Eplerenone Implantation Improved Adipose Dysfunction Averting RAAS Activation and Cell Division
(2020) Vecchiola Cárdenas, Andrea Paola; Fuentes, C. A.; Solar, I.; Lagos, C. F.; Opazo, M. C.; Muñoz Durango, Natalia; Riedel Soria, Claudia; Owen, Gareth Ivor; Kalergis Parra, Alexis Mikes; Fardella B., Carlos
Evaluation of the chemopreventive potentials of ezetimibe and aspirin in a novel mouse model of gallbladder preneoplasia
(2020) Rosa, L.; Muñoz Durango, Natalia; García Cañete, Patricia; Bizama, Carolina; González Briones, Ximena María; Wichmann Pérez, Ignacio Alberto; Arrese, Marco; Ferreccio Readi, Catterina; Kalergis Parra, Alexis Mikes; Miquel P., Juan Francisco; Roa Strauch, Juan Carlos Enrique; Lobos-Gonzalez, L.; Gomez, N.; Saavedra, N.; Guevara, F.; Villegas, J.; Espinoza, J. A.
Immune System Alterations by Aldosterone During Hypertension : From Clinical Observations to Genomic and Non-Genomic Mechanisms Leading to Vascular Damage
(2013) Muñoz Durango, Natalia; Barake Sabbagh, M. Francisca; Letelier, N.; Campino Johnson, María del Carmen; Fardella B., Carlos; Kalergis Parra, Alexis Mikes
Interleukin-10 plays a key role in the modulation of neutrophils recruitment and lung inflammation during infection by Streptococcus pneumoniae
(2015) Peñaloza, Hernán F.; Nieto Pacheco, Pamela Andrea; Muñoz Durango, Natalia; Salazar Echegarai, Francisco Javier; Torres Montes, Paula Javiera; Parga Ponce, María José; Álvarez Lobos, Manuel; Riedel, Claudia A.; Kalergis Parra, Alexis Mikes; Bueno Ramírez, Susan
Interleukin-10 Production by T and B Cells Is a Key Factor to Promote Systemic Salmomnella enterica Serovar Typhimurium Infection in Mice
(2017) Salazar Tapia, Geraldyne Alessandra; Peñaloza Cerda, Hernán F.; Pardo Roa, Catalina; Schultz Lombardic, Bárbara M.; Muñoz Durango, Natalia; Gómez Johnson, Roberto Sebastián; Salazar Echegarai, Francisco Javier; Pizarro Solar, Daniela Paz; Riedel, Claudia A.; González Muñoz, Pablo Alberto; Álvarez Lobos, Manuel; Kalergis Parra, Alexis Mikes; Bueno Ramírez, Susan
Salmonella enterica serovar Typhimurium (S. Typhimurium) is a Gram-negative bacterium that produces disease in numerous hosts. In mice, oral inoculation is followed by intestinal colonization and subsequent systemic dissemination, which leads to severe pathogenesis without the activation of an efficient anti-Salmonella immune response. This feature suggests that the infection caused by S. Typhimurium may promote the production of anti-inflammatory molecules by the host that prevent efficient T cell activation and bacterial clearance. In this study, we describe the contribution of immune cells producing the anti-inflammatory cytokine interleukin-10 (IL-10) to the systemic infection caused by S. Typhimurium in mice. We observed that the production of IL-10 was required by S. Typhimurium to cause a systemic disease, since mice lacking IL-10 (IL-10(-/-)) were significantly more resistant to die after an infection as compared to wild-type (WT) mice. IL-10(-/-) mice had reduced bacterial loads in internal organs and increased levels of pro-inflammatory cytokines in serum at 5 days of infection. Importantly, WT mice showed high bacterial loads in tissues and no increase of cytokines in serum after 5 days of S. Typhimurium infection, except for IL-10. In WT mice, we observed a peak of il-10 messenger RNA production in ileum, spleen, and liver after 5 days of infection. Importantly, the adoptive transfer of T or B cells from WT mice restored the susceptibility of IL-10(-/-) mice to systemic S. Typhimurium infection, suggesting that the generation of regulatory cells in vivo is required to sustain a systemic infection by S. Typhimurium. These findings support the notion that IL-10 production from lymphoid cells is a key process in the infective cycle of S. Typhimurium in mice due to generation of a tolerogenic immune response that prevents bacterial clearance and supports systemic dissemination.
Patterns of antibody response during natural hRSV infection : insights for the development of new antibody-based therapies
(2018) Muñoz Durango, Natalia; Pizarro Ortega, Magdalena S.; Rey Jurado, Emma; Díaz Acevedo, Fabián Esteban; Bueno Ramírez, Susan; Kalergis Parra, Alexis Mikes
Peripheral Blood Classical Monocytes and Plasma Interleukin 10 Are Associated to Neoadjuvant Chemotherapy Response in Breast Cancer Patients
(2020) Valdés Ferrada, J.; Muñoz Durango, Natalia; Pérez Sepúlveda, Alejandra Andrea; Muniz, S.; Coronado Arrázola, Irenice; Acevedo Claros, Francisco Nicolás; Muñoz Soto, Jorge; Bueno Ramírez, Susan; Sánchez Rojel, César Giovanni; Kalergis Parra, Alexis Mikes
Safety and immunogenicity evaluation of recombinant BCG vaccine against respiratory syncytial virus in a randomized, double-blind, placebo-controlled phase I clinical trial
(2020) Abarca Villaseca, Katia; Rey Jurado, Emma; Muñoz Durango, Natalia; Soto Ramírez, Jorge Andrés; Gálvez Arriagada, Nicolás Marcelo Salvador; Borzutzky Schachter, Arturo; Cerda, Jaime; Villarroel del Pino, Luis A.; González Muñoz, Pablo Alberto; González Aramundiz, José Vicente; Bueno Ramírez, Susan; Kalergis Parra, Alexis Mikes; Valdés-Ferrada, J.; Iturriaga, C.; Urzúa, M.; Madrid, V.; Bueno Ramírez, Susan; Vázquez, Y.
The role of myeloid-derived suppressor cells in chronic infectious diseases and the current methodology available for their study
(2019) Peñaloza Cerda, Hernán F.; Álvarez Espejo, Diana Claudia Marcela; Muñoz Durango, Natalia; Schultz Lombardic, Bárbara M.; González, Pablo A.; Kalergis Parra, Alexis Mikes; Bueno Ramírez, Susan
An effective pathogen has the ability to evade the immune response. The strategies used to achieve this may be based on the direct action of virulence factors or on the induction of host factors. Myeloid-derived suppressor cells (MDSCs) are immune cells with an incredible ability to suppress the inflammatory response, which makes them excellent targets to be exploited by pathogenic bacteria, viruses, or parasites. In this review, we describe the origin and suppressive mechanisms of MDSCs, as well as their role in chronic bacterial, viral, and parasitic infections, where their expansion seems to be essential in the chronicity of the disease. We also analyze the disadvantages of current MDSC depletion strategies and the different in vitro generation methods, which can be useful tools for the deeper study of these cells in the context of microbial infections.
Unraveling the immune function of mineralocorticoid receptor (MR) and aldosterone in animal models.
(2019) Muñoz Durango, Natalia; Kalergis Parra, Alexis Mikes; Pontificia Universidad Católica de Chile. Facultad de Ciencias Biológicas
Inflammation is a physiological response that could be triggered by endogenous and exogenous stimulus. During inflammation the response is auto limited and regulated to keep homeostasis, because uncontrolled response could lead to death. Inflammatory response is complex and involves many systems of the body which crosstalk each with other. In this line, hormones and its cognate receptors have been described as modulator of immune response, for example glucocorticoids and its knowing immunosuppressive role have been very useful to treat cancer and autoimmune diseases. Aldosterone is another adrenal hormone, that under non-pathological condition controls renal excretion of water and electrolytes to keep blood pressure. This hormone conventionally acts through mineralocorticoid receptor (MR) which is a ligand dependent transcription factor mainly expressed in juxtaglomerular epithelial cells in kidneys. However, MR is also expressed in cells of the immune system, adipose tissue, liver and brain, indicating that could be paying a role. Up to date, it has been described that high levels of aldosterone in vivo and in vitro are related with the induction of inflammatory phenotype in cardiac diseases, atherosclerosis, obesity, insulin resistance and autoimmunity. Aimed to describe the immunological role in which MR and aldosterone are involved, we used two models to study it. The first model was designed to understand whether MRaldosterone was related with TLR4 expression. According to our findings we described that aldosterone via MR induces the expression of tlr4 in wild type (WT) bone marrow-derived dendritic cells (DCs). Oppositely, the trl4 expression in DCs derived from myeloid MR conditional knockout mice (MyMRKO) did not show to be modulated by aldosterone, indeed these cells displayed impaired capacity to response to LPS stimulation. Finally, in a model of sub-lethal endotoxemia, we found that mice pre-treated with aldosterone succumbs after LPS challenge in contrast to placebo treated mice, mainly due to a multi-organic failure. In conclusion our results suggest that aldosterone-MR axis is involved in the regulation of tlr4 expression, and in consequently modulating the DCs response to TLR4 agonist, LPS. Because the first model was focused in septic inflammation, the second model that we used was focused in aseptic chronic inflammation in which MR and renin-angiotensinaldosterone system (RAAS) played a role. We induced non-alcoholic steatohepatitis (NASH) in LM/WT and MyMRKO mice with methionine-choline deficient diet (MCD). We found that MyMRKO mice fed with MCD diet presented lower lipid accumulation in livers than controls. This finding was also related with lower number of CD8+ T lymphocytes infiltration in livers of MyMRKO. This cells also displayed lower expression CD25 activation receptor, indicating that antigen presenting cells (APC) derived from MyMRKO could be having impairments promoting the immune response. In vitro cocultures performed with CD4+ or CD8+ T lymphocytes plus DCs derived from MyMRKO mice displayed that only CD8+ response was impaired and is related with the phenotype seen in mice. Summarizing the results, we described that aldosterone through MR are involved in tlr4 expression, because the loss of MR in myeloid DCs impacted in the levels of tlr4 expressed, indeed at basal condition. This result also affected the capacity of MyMRKO DCs to sense and responds to LPS, which is a maturation stimulus, but in these cells failed to induced a proinflammatory prone phenotype. These results are in accordance with the lowest capacity of DCs to drive immune response of CD8+ T lymphocytes impacting in lower steatosis in NASH model. In conclusion, all abovementioned results indicated that loss of MR in myeloid cells impacts in the adaptive CD8+ immune response. However, further analysis about how MR modulates antigen presenting cells to impair CD8+ T lymphocytes function is needed.Inflammation is a physiological response that could be triggered by endogenous and exogenous stimulus. During inflammation the response is auto limited and regulated to keep homeostasis, because uncontrolled response could lead to death. Inflammatory response is complex and involves many systems of the body which crosstalk each with other. In this line, hormones and its cognate receptors have been described as modulator of immune response, for example glucocorticoids and its knowing immunosuppressive role have been very useful to treat cancer and autoimmune diseases. Aldosterone is another adrenal hormone, that under non-pathological condition controls renal excretion of water and electrolytes to keep blood pressure. This hormone conventionally acts through mineralocorticoid receptor (MR) which is a ligand dependent transcription factor mainly expressed in juxtaglomerular epithelial cells in kidneys. However, MR is also expressed in cells of the immune system, adipose tissue, liver and brain, indicating that could be paying a role. Up to date, it has been described that high levels of aldosterone in vivo and in vitro are related with the induction of inflammatory phenotype in cardiac diseases, atherosclerosis, obesity, insulin resistance and autoimmunity. Aimed to describe the immunological role in which MR and aldosterone are involved, we used two models to study it. The first model was designed to understand whether MRaldosterone was related with TLR4 expression. According to our findings we described that aldosterone via MR induces the expression of tlr4 in wild type (WT) bone marrow-derived dendritic cells (DCs). Oppositely, the trl4 expression in DCs derived from myeloid MR conditional knockout mice (MyMRKO) did not show to be modulated by aldosterone, indeed these cells displayed impaired capacity to response to LPS stimulation. Finally, in a model of sub-lethal endotoxemia, we found that mice pre-treated with aldosterone succumbs after LPS challenge in contrast to placebo treated mice, mainly due to a multi-organic failure. In conclusion our results suggest that aldosterone-MR axis is involved in the regulation of tlr4 expression, and in consequently modulating the DCs response to TLR4 agonist, LPS. Because the first model was focused in septic inflammation, the second model that we used was focused in aseptic chronic inflammation in which MR and renin-angiotensinaldosterone system (RAAS) played a role. We induced non-alcoholic steatohepatitis (NASH) in LM/WT and MyMRKO mice with methionine-choline deficient diet (MCD). We found that MyMRKO mice fed with MCD diet presented lower lipid accumulation in livers than controls. This finding was also related with lower number of CD8+ T lymphocytes infiltration in livers of MyMRKO. This cells also displayed lower expression CD25 activation receptor, indicating that antigen presenting cells (APC) derived from MyMRKO could be having impairments promoting the immune response. In vitro cocultures performed with CD4+ or CD8+ T lymphocytes plus DCs derived from MyMRKO mice displayed that only CD8+ response was impaired and is related with the phenotype seen in mice. Summarizing the results, we described that aldosterone through MR are involved in tlr4 expression, because the loss of MR in myeloid DCs impacted in the levels of tlr4 expressed, indeed at basal condition. This result also affected the capacity of MyMRKO DCs to sense and responds to LPS, which is a maturation stimulus, but in these cells failed to induced a proinflammatory prone phenotype. These results are in accordance with the lowest capacity of DCs to drive immune response of CD8+ T lymphocytes impacting in lower steatosis in NASH model. In conclusion, all abovementioned results indicated that loss of MR in myeloid cells impacts in the adaptive CD8+ immune response. However, further analysis about how MR modulates antigen presenting cells to impair CD8+ T lymphocytes function is needed.Inflammation is a physiological response that could be triggered by endogenous and exogenous stimulus. During inflammation the response is auto limited and regulated to keep homeostasis, because uncontrolled response could lead to death. Inflammatory response is complex and involves many systems of the body which crosstalk each with other. In this line, hormones and its cognate receptors have been described as modulator of immune response, for example glucocorticoids and its knowing immunosuppressive role have been very useful to treat cancer and autoimmune diseases. Aldosterone is another adrenal hormone, that under non-pathological condition controls renal excretion of water and electrolytes to keep blood pressure. This hormone conventionally acts through mineralocorticoid receptor (MR) which is a ligand dependent transcription factor mainly expressed in juxtaglomerular epithelial cells in kidneys. However, MR is also expressed in cells of the immune system, adipose tissue, liver and brain, indicating that could be paying a role. Up to date, it has been described that high levels of aldosterone in vivo and in vitro are related with the induction of inflammatory phenotype in cardiac diseases, atherosclerosis, obesity, insulin resistance and autoimmunity. Aimed to describe the immunological role in which MR and aldosterone are involved, we used two models to study it. The first model was designed to understand whether MRaldosterone was related with TLR4 expression. According to our findings we described that aldosterone via MR induces the expression of tlr4 in wild type (WT) bone marrow-derived dendritic cells (DCs). Oppositely, the trl4 expression in DCs derived from myeloid MR conditional knockout mice (MyMRKO) did not show to be modulated by aldosterone, indeed these cells displayed impaired capacity to response to LPS stimulation. Finally, in a model of sub-lethal endotoxemia, we found that mice pre-treated with aldosterone succumbs after LPS challenge in contrast to placebo treated mice, mainly due to a multi-organic failure. In conclusion our results suggest that aldosterone-MR axis is involved in the regulation of tlr4 expression, and in consequently modulating the DCs response to TLR4 agonist, LPS. Because the first model was focused in septic inflammation, the second model that we used was focused in aseptic chronic inflammation in which MR and renin-angiotensinaldosterone system (RAAS) played a role. We induced non-alcoholic steatohepatitis (NASH) in LM/WT and MyMRKO mice with methionine-choline deficient diet (MCD). We found that MyMRKO mice fed with MCD diet presented lower lipid accumulation in livers than controls. This finding was also related with lower number of CD8+ T lymphocytes infiltration in livers of MyMRKO. This cells also displayed lower expression CD25 activation receptor, indicating that antigen presenting cells (APC) derived from MyMRKO could be having impairments promoting the immune response. In vitro cocultures performed with CD4+ or CD8+ T lymphocytes plus DCs derived from MyMRKO mice displayed that only CD8+ response was impaired and is related with the phenotype seen in mice. Summarizing the results, we described that aldosterone through MR are involved in tlr4 expression, because the loss of MR in myeloid DCs impacted in the levels of tlr4 expressed, indeed at basal condition. This result also affected the capacity of MyMRKO DCs to sense and responds to LPS, which is a maturation stimulus, but in these cells failed to induced a proinflammatory prone phenotype. These results are in accordance with the lowest capacity of DCs to drive immune response of CD8+ T lymphocytes impacting in lower steatosis in NASH model. In conclusion, all abovementioned results indicated that loss of MR in myeloid cells impacts in the adaptive CD8+ immune response. However, further analysis about how MR modulates antigen presenting cells to impair CD8+ T lymphocytes function is needed.

Browsing by Author "Muñoz Durango, Natalia"

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