Browsing by Author "Riedel Soria, Claudia"

Now showing 1 - 12 of 12
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    Activating and inhibitory Fc gamma receptors can differentially modulate T cell-mediated autoimmunity
    (2008) Iruretagoyena B., Mirentxu; Riedel Soria, Claudia; Leiva Llantén, Eduardo David; Gutiérrez Torres, Miguel Alejandro; Jacobelli, Sergio H.; Kalergis Parra, Alexis Mikes
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    Advances in understanding respiratory syncytial virus infection in airway epithelial cells and consequential effects on the immune response
    (2013) Bueno Ramírez, Susan Marcela; Cespedes Donoso, Pablo Francisco; González, Pablo A.; Kalergis Parra, Alexis Mikes; Lay Remolcoi, Margarita Kam-len; León, Miguel A.; Riedel Soria, Claudia
    This article reviews aspects of respiratory syncytial virus (RSV) infection in airway epithelial cells (AECs), including cytopathogenesis, entry, replication and the induction of immune response to the virus, including a new role for thymic stromal lymphopoietin in RSV immunopathology. (C) 2012 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
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    Asymptomatic Herpes Simplex Virus Type 1 Infection Causes an Earlier Onset and More Severe Experimental Autoimmune Encephalomyelitis
    (2021) Duarte Peñaloza, Luisa Fernanda; Altamirano Lagos, María J.; Tabares Guevara, Jorge H.; Opazo, María Cecilia; Díaz, Máximo; Navarrete, Romina; Muza, Catalina; Vallejos Galvez, Omar Patricio; Riedel Soria, Claudia; Bueno Ramírez, Susan; Kalergis Parra, Alexis Mikes; González Muñoz, Pablo Alberto
    Multiple sclerosis (MS) is an increasingly prevalent progressive autoimmune and debilitating chronic disease that involves the detrimental recognition of central nervous system (CNS) antigens by the immune system. Although significant progress has been made in the last decades on the biology of MS and the identification of novel therapies to treat its symptoms, the etiology of this disease remains unknown. However, recent studies have suggested that viral infections may contribute to disease onset. Interestingly, a potential association between herpes simplex virus type 1 (HSV-1) infection and MS has been reported, yet a direct relationship among both has not been conclusively demonstrated. Experimental autoimmune encephalomyelitis (EAE) recapitulates several aspects of MS in humans and is widely used to study this disease. Here, we evaluated the effect of asymptomatic brain infection by HSV-1 on the onset and severity of EAE in C57BL/6 mice. We also evaluated the effect of infection with an HSV-1-mutant that is attenuated in neurovirulence and does not cause encephalitis. Importantly, we observed more severe EAE in mice previously infected either, with the wild-type (WT) or the mutant HSV-1, as compared to uninfected control mice. Also, earlier EAE onset was seen after WT virus inoculation. These findings support the notion that a previous exposure to HSV-1 can accelerate and enhance EAE, which suggests a potential contribution of asymptomatic HSV-1 to the onset and severity of MS.
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    BCG-induced cross-protection and development of trained immunity: implication for vaccine design
    (2019) Covián, Camila; Fernández Fierro, Ayleen Lorena; Retamal Díaz, Angello Ricardo; Díaz Acevedo, Fabián Esteban; Vásquez Veloso, Abel; Lay Remolcoi, Margarita Kam-len; Riedel Soria, Claudia; González Muñoz, Pablo Alberto; Bueno Ramírez, Susan; Kalergis Parra, Alexis Mikes
    The Bacillus Calmette-Guerin (BCG) is a live attenuated tuberculosis vaccine that has the ability to induce non-specific cross-protection against pathogens that might be unrelated to the target disease. Vaccination with BCG reduces mortality in newborns and induces an improved innate immune response against microorganisms other than Mycobacterium tuberculosis, such as Candida albicans and Staphylococcus aureus. Innate immune cells, including monocytes and natural killer (NK) cells, contribute to this non-specific immune protection in a way that is independent of memory T or B cells. This phenomenon associated with a memory-like response in innate immune cells is known as "trained immunity." Epigenetic reprogramming through histone modification in the regulatory elements of particular genes has been reported as one of the mechanisms associated with the induction of trained immunity in both, humans and mice. Indeed, it has been shown that BCG vaccination induces changes in the methylation pattern of histones associated with specific genes in circulating monocytes leading to a "trained" state. Importantly, these modifications can lead to the expression and/or repression of genes that are related to increased protection against secondary infections after vaccination, with improved pathogen recognition and faster inflammatory responses. In this review, we discuss BCG-induced cross-protection and acquisition of trained immunity and potential heterologous effects of recombinant BCG vaccines.
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    Chromosomal excision of a new pathogenicity island modulates Salmonella virulence in vivo
    (BENTHAM SCIENCE PUBL LTD, 2013) Tobar Durán, Hugo Eduardo; Salazar Echegarai, Francisco J.; Nieto Pacheco, Pamela Andrea; Palavecino, Christian E.; Sebastian, Vatenlina P.; Riedel Soria, Claudia; Kalergis Parra, Alexis Mikes; Bueno Ramírez, Susan
    Although the excision of unstable pathogenicity islands is a phenomenon that has been described for several virulent bacteria, whether this process directly affects the capacity of these microorganisms to cause disease in their hosts remains unknown. Salmonella enterica serovar Enteritidis (S. Enteritidis) is an enterobacterium that harbors several unstable pathogenicity islands that can excise from the main bacterial chromosome. Here we have evaluated whether excision of one of these pathogenicity islands, denominated as Region of Difference 21 (ROD21), is required for S. Enteritidis to cause disease in the host. By means of genetic targeting of the integrase encoded by the ROD21 we have generated S. Enteritidis strains unable to excise ROD21. The failure to excise ROD21 significantly reduced the capacity to cause a lethal disease and to colonize the spleen and liver of mice, as compared to wild type S. Enteritidis. On the contrary, S. Enteritidis strains overexpressing an excisionase protein increased the frequency of ROD21 excision and showed an improved capacity to cause lethal disease in mice. Accordingly, strains unable to excise ROD21 showed an altered expression of genes located in this pathogenicity island. Our results suggest that the genetic excision of the pathogenicity island ROD21 in S. Enteritidis modulates the capacity of this bacterium to cause disease in mice due to a change in the expression of virulence genes.
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    Crosstalk Between Epithelial Cells, Neurons and Immune Mediators in HSV-1 Skin Infection
    (2021) Duarte Peñaloza, Luisa Fernanda; Reyes Muñoz, Antonia; Farías León, Mónica; Riedel Soria, Claudia; Bueno Ramírez, Susan; Kalergis Parra, Alexis; González Adonis, Pablo Andrés
    Herpes simplex virus type 1 (HSV-1) infection is highly prevalent in humans, with approximately two-thirds of the world population living with this virus. However, only a fraction of those carrying HSV-1, which elicits lifelong infections, are symptomatic. HSV-1 mainly causes lesions in the skin and mucosae but reaches the termini of sensory neurons innervating these tissues and travels in a retrograde manner to the neuron cell body where it establishes persistent infection and remains in a latent state until reactivated by different stimuli. When productive reactivations occur, the virus travels back along axons to the primary infection site, where new rounds of replication are initiated in the skin, in recurrent or secondary infections. During this process, new neuron infections occur. Noteworthy, the mechanisms underlying viral reactivations and the exit of latency are somewhat poorly understood and may be regulated by a crosstalk between the infected neurons and components of the immune system. Here, we review and discuss the immune responses that occur at the skin during primary and recurrent infections by HSV-1, as well as at the interphase of latently-infected neurons. Moreover, we discuss the implications of neuronal signals over the priming and migration of immune cells in the context of HSV-1 infection.
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    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
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    Heme Oxygenase-1 Expression in Dendritic Cells Contributes to Protective Immunity against Herpes Simplex Virus Skin Infection
    (MDPI, 2023) Tognarelli Torres, Eduardo Ignacio; Duarte Peñaloza, Luisa Fernanda; Farías León, Mónica Andrea; Cancino Prado, Felipe Andrés; Corrales Bonilla, Nicolas; Ibañez Irribarra, Francisco Javier; Riedel Soria, Claudia; Bueno Ramírez, Susan; Kalergis Parra,Alexis Mikes; González Muñoz, Pablo Alberto
    Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) infections are highly prevalent in the human population and produce mild to life-threatening diseases. These viruses interfere with the function and viability of dendritic cells (DCs), which are professional antigen-presenting cells that initiate and regulate the host's antiviral immune responses. Heme oxygenase-1 (HO-1) is an inducible host enzyme with reported antiviral activity against HSVs in epithelial cells and neurons. Here, we sought to assess whether HO-1 modulates the function and viability of DCs upon infection with HSV-1 or HSV-2. We found that the stimulation of HO-1 expression in HSV-inoculated DCs significantly recovered the viability of these cells and hampered viral egress. Furthermore, HSV-infected DCs stimulated to express HO-1 promoted the expression of anti-inflammatory molecules, such as PDL-1 and IL-10, and the activation of virus-specific CD4(+) T cells with regulatory (Treg), Th17 and Treg/Th17 phenotypes. Moreover, HSV-infected DCs stimulated to express HO-1 and then transferred into mice, promoted the activation of virus-specific T cells and improved the outcome of HSV-1 skin infection. These findings suggest that stimulation of HO-1 expression in DCs limits the deleterious effects of HSVs over these cells and induces a favorable virus-specific immune response in the skin against HSV-1.
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    Herpes Simplex Virus Type 1 Infection of the Central Nervous System : Insights Into Proposed Interrelationships With Neurodegenerative Disorders
    (2019) Duarte Peñaloza, Luisa Fernanda; Farías León, Mónica Andrea; Álvarez Espejo, Diana Claudia Marcela; Bueno Ramírez, Susan; Riedel Soria, Claudia; González Muñoz, Pablo Alberto; Gonzalez-Dunia, Daniel
    Herpes simplex virus type 1 (HSV-1) is highly prevalent in humans and can reach the brain without evident clinical symptoms. Once in the central nervous system (CNS), the virus can either reside in a quiescent latent state in this tissue, or eventually actively lead to severe acute necrotizing encephalitis, which is characterized by exacerbated neuroinflammation and prolonged neuroimmune activation producing a life-threatening disease. Although HSV-1 encephalitis can be treated with antivirals that limit virus replication, neurological sequelae are common and the virus will nevertheless remain for life in the neural tissue. Importantly, there is accumulating evidence that suggests that HSV-1 infection of the brain both, in symptomatic and asymptomatic individuals could lead to neuronal damage and eventually, neurodegenerative disorders. Here, we review and discuss acute and chronic infection of particular brain regions by HSV-1 and how this may affect neuron and cognitive functions in the host. We review potential cellular and molecular mechanisms leading to neurodegeneration, such as protein aggregation, dysregulation of autophagy, oxidative cell damage and apoptosis, among others. Furthermore, we discuss the impact of HSV-1 infection on brain inflammation and its potential relationship with neurodegenerative diseases.
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    Mechanisms used by virulent Salmonella to impair dendritic cell function and evade adaptive immunity
    (2012) Bueno Ramírez, Susan; Riquelme Colet, Sebastián Alejandro; Riedel Soria, Claudia; Kalergis Parra, Alexis Mikes
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    Naturally derived heme-oxygenase 1 inducers and their therapeutic application to immune-mediated diseases
    (Frontiers Media S.A., 2020) Funes, Samanta Celeste; Rios Raggio, Mariana; Fernández Fierro, Ayleen Lorena; Covián, Camila; Bueno Ramírez, Susan; Riedel Soria, Claudia; Mackern Oberti, Juan Pablo; Kalergis Parra, Alexis Mikes
    Heme oxygenase (HO) is the primary antioxidant enzyme involved in heme group degradation. A variety of stimuli triggers the expression of the inducible HO-1 isoform, which is modulated by its substrate and cellular stressors. A major anti-inflammatory role has been assigned to the HO-1 activity. Therefore, in recent years HO-1 induction has been employed as an approach to treating several disorders displaying some immune alterations components, such as exacerbated inflammation or self-reactivity. Many natural compounds have shown to be effective inductors of HO-1 without cytotoxic effects; among them, most are chemicals present in plants used as food, flavoring, and medicine. Here we discuss some naturally derived compounds involved in HO-1 induction, their impact in the immune response modulation, and the beneficial effect in diverse autoimmune disorders. We conclude that the use of some compounds from natural sources able to induce HO-1 is an attractive lifestyle toward promoting human health. This review opens a new outlook on the investigation of naturally derived HO-1 inducers, mainly concerning autoimmunity.
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    Virulence Mechanisms Displayed by Salmonella to Impair Dendritic Cell Function
    (2010) Bueno Ramírez, Susan; Riedel Soria, Claudia; Carreño Márquez, Leandro Javier; Kalergis Parra, Alexis Mikes