Examinando por Autor "Riedel, Claudia A"

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    BCG-Induced Cross-Protection and Development of Trained Immunity: Implication for Vaccine Design
    (Frontiers Media S.A., 2019-11) Covián, Camilaa; Fernández-Fierro, Ayleen; Retamal-Díaz, Angello; Díaz, Fabián E; Vasquez, Abel E.; Lay, Margarita K; Riedel, Claudia A; González, Pablo A; Bueno, Susan M.; Kalergis, Alexis M
    The Bacillus Calmette-Guérin (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. © Copyright © 2019 Covián, Fernández-Fierro, Retamal-Díaz, Díaz, Vasquez, Lay, Riedel, González, Bueno and Kalergis.
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    Cytokines in the respiratory airway as biomarkers of severity and prognosis for respiratory syncytial virus infection: An update
    (Frontiers Media S.A., 2019-06) Vázquez, Yaneisi; González, Liliana; Loreani, Noguera; González, Pablo A; Riedel, Claudia A; Bertrand, Pablo; Bueno, Susan M
    The human respiratory syncytial virus (hRSV) is one of the most important causes of upper and lower respiratory tract infections in children and the main cause of bronchiolitis worldwide. Disease manifestations caused by hRSV may vary from mild to severe, occasionally requiring admission and hospitalization in intensive care units. Despite the high morbidity rates associated to bronchiolitis, treatment options against hRSV are limited and there are no current vaccination strategies to prevent infection. Importantly, the early identification of high-risk patients can help improve disease management and prevent complications associated with hRSV infection. Recently, the characterization of pro- and anti-inflammatory cytokine patterns produced during hRSV-related inflammatory processes has allowed the identification of potential prognosis biomarkers. A suitable biomarker should allow predicting the severity of the infection in a simple and opportune manner and should ideally be obtained from non-invasive samples. Among the cytokines associated with hRSV disease severity, IL-8, interferon-alpha (IFN-alpha), and IL-6, as well as the Th2-type cytokines thymic stromal lymphopoietin (TSLP), IL-3, and IL-33 have been highlighted as molecules with prognostic value in hRSV infections. In this review, we discuss current studies that describe molecules produced by patients during hRSV infection and their potential as biomarkers to anticipate the severity of the disease caused by this virus. © 2019 Vázquez, González, Noguera, González, Riedel, Bertrand and Bueno.
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    Herpes simplex virus type 1 infection of the central nervous system: Insights into proposed interrelationships with neurodegenerative disorders
    (Frontiers Media S.A., 2019-01) Duarte, Luisa; Farías, Mónica A; Álvarez, Diana M; Bueno, Susan M; Riedel, Claudia A; González, Pablo A
    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. © 2019 Duarte, Farías, Álvarez, Bueno, Riedel and González.