Browsing by Author "Pizarro-Ortega, Magdalena S."

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    Contribution of Cytokines to Tissue Damage During Human Respiratory Syncytial Virus Infection.
    (2019) Bohmwald, Karen; Gálvez, Nicolás M. S.; Canedo-Marroquín, Gisela; Pizarro-Ortega, Magdalena S.; Andrade-Parra, Catalina; Gómez-Santander, Felipe; Kalergis, Alexis M.
    The human respiratory syncytial virus (hRSV) remains one of the leading pathogens causing acute respiratory tract infections (ARTIs) in children younger than 2 years old, worldwide. Hospitalizations during the winter season due to hRSV-induced bronchiolitis and pneumonia increase every year. Despite this, there are no available vaccines to mitigate the health and economic burden caused by hRSV infection. The pathology caused by hRSV induces significant damage to the pulmonary epithelium, due to an excessive inflammatory response at the airways. Cytokines are considered essential players for the establishment and modulation of the immune and inflammatory responses, which can either be beneficial or harmful for the host. The deleterious effect observed upon hRSV infection is mainly due to tissue damage caused by immune cells recruited to the site of infection. This cellular recruitment takes place due to an altered profile of cytokines secreted by epithelial cells. As a result of inflammatory cell recruitment, the amounts of cytokines, such as IL-1, IL-6, IL-10, and CCL5 are further increased, while IL-10 and IFN-γ are decreased. However, additional studies are required to elicit the mediators directly associated with hRSV damage entirely. In addition to the detrimental induction of inflammatory mediators in the respiratory tract caused by hRSV, reports indicating alterations in the central nervous system (CNS) have been published. Indeed, elevated levels of IL-6, IL-8 (CXCL8), CCL2, and CCL4 have been reported in cerebrospinal fluid from patients with severe bronchiolitis and hRSV-associated encephalopathy. In this review article, we provide an in-depth analysis of the role of cytokines secreted upon hRSV infection and their potentially harmful contribution to tissue damage of the respiratory tract and the CNS.
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    Immunological Features of Respiratory Syncytial Virus-Caused Pneumonia-Implications for Vaccine Design.
    (2017) Rey-Jurado, Emma; Pizarro-Ortega, Magdalena S.; Kalergis, Alexis M.
    The human respiratory syncytial virus (hRSV) is the causative agent for high rates of hospitalizations due to viral bronchiolitis and pneumonia worldwide. Such a disease is characterized by an infection of epithelial cells of the distal airways that leads to inflammation and subsequently to respiratory failure. Upon infection, different pattern recognition receptors recognize the virus and trigger the innate immune response against the hRSV. Further, T cell immunity plays an important role for virus clearance. Based on animal studies, it is thought that the host immune response to hRSV is based on a biased T helper (Th)-2 and Th17 T cell responses with the recruitment of T cells, neutrophils and eosinophils to the lung, causing inflammation and tissue damage. In contrast, human immunity against RSV has been shown to be more complex with no definitive T cell polarization profile. Nowadays, only a humanized monoclonal antibody, known as palivizumab, is available to protect against hRSV infection in high-risk infants. However, such treatment involves several injections at a significantly high cost. For these reasons, intense research has been focused on finding novel vaccines or therapies to prevent hRSV infection in the population. Here, we comprehensively review the recent literature relative to the immunological features during hRSV infection, as well as the new insights into preventing the disease caused by this virus.
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    Insights on the crosstalk between dendritic cells and helper T cells in novel genetic etiology for mendelian susceptible mycobacterial disease.
    (2018) Rey-Jurado, Emma; Pizarro-Ortega, Magdalena S.; Kalergis, Alexis M.; Mendelian susceptibility to mycobacterial disease (MSMD) is an inherited predisposition to infections by Bacille-Calmette Guérin (BCG) vaccine or by environmental mycobacteria. The etiology of MSMD has been associated with up to nineteen different genetic mutations in interferon (IFN)-γ-related genes.1 Although mycobacteria susceptibility-associated genetic mutations are rare in the population, their diagnosis is crucial for an efficient and timely treatment. Kong et al.2 have recently described an autosomal recessive deficiency in the signal.