Browsing by Author "Vazquez, Yaneisi"

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    Evaluation of monoclonal antibodies that detect conserved proteins from Respiratory Syncytial Virus, Metapneumovirus and Adenovirus in human samples
    (2018) González Carreño, Liliana Andrea; Vazquez, Yaneisi; Mora, Jorge E.; Palavecino, Christian E.; Bertrand N., Pablo; Ferrés Garrido, Marcela Viviana; Contreras, Ana María; Beckhaus, Andrea A.; Riedel, Claudia; Bueno Ramírez, Susan
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    Identification of biomarkers for disease severity in nasopharyngeal secretions of infants with upper or lower respiratory tract viral infections
    Bertrand N., Pablo; Vazquez, Yaneisi; Beckhaus, Andrea A.; González Carreño, Liliana Andrea; Contreras Sepúlveda, Ana María; Ferrés Garrido, Marcela Viviana; Padilla Pérez, Oslando; Riedel, Claudia A.; Kalergis Parra, Alexis Mikes; Bueno, Susan M.
    Lower respiratory tract infections (LRTIs) produced by viruses are the most frequent cause of morbidity and mortality in children younger than 5 years of age. The immune response triggered by viral infection can induce a strong inflammation in the airways and cytokines could be considered as biomarkers for disease severity as these molecules modulate the inflammatory response that defines the outcome of patients. Aiming to predict the severity of disease during respiratory tract infections, we conducted a 1-year follow-up observational study in infants who presented upper or lower respiratory tract infections caused by seasonal respiratory viruses. At the time of enrollment, nasopharyngeal swabs (NPS) were obtained from infants to measure mRNA expression and protein levels of IL-3, IL-8, IL-33, and thymic stromal lymphopoietin. While all cytokines significantly increased their protein levels in infants with upper and lower respiratory tract infections as compared to control infants, IL-33 and IL-8 showed a significant increase in respiratory syncytial virus (RSV)-infected patients with LRTI as compared to patients with upper respiratory tract infection. We also found higher viral loads of RSV-positive samples with a greater IL-8 response at the beginning of the symptoms. Data obtained in this study suggest that both IL-8 and IL-33 could be used as biomarkers for clinical severity for infants suffering from LRTIs caused by the RSV.
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    Interleukin-10 Produced by Myeloid-Derived Suppressor Cells Provides Protection to Carbapenem-Resistant Klebsiella pneumoniae Sequence Type 258 by Enhancing Its Clearance in the Airways
    (2019) Peñaloza Cerda, Hernán F.; Noguera Mijares, Loreani Paola; Ahn, D.; Vallejos, Omar; Castellanos, Raquel M.; Vazquez, Yaneisi; Salazar Echegarai, Francisco Javier; González Carreño, Liliana; Suazo Gálvez, Isidora del Carmen; Pardo Roa, Catalina; Salazar, Geraldyne; Prince, Alice; Bueno Ramírez, Susan
    Carbapenem-resistant Klebsiella pneumoniae sequence type 258 (CRKP-ST258) can cause chronic infections in lungs and airways, with repeated episodes of bacteremia. In this report we addressed whether the recruitment of myeloid cells producing the anti-inflammatory cytokine interleukin-10 (IL-10) modulates the clearance of CKRP-ST258 in the lungs and establishes bacterial persistence. Our data demonstrate that during pneumonia caused by a clinical isolate of CRKP-ST258 (KP35) there is an early recruitment of monocyte-myeloid-derived suppressor cells (M-MDSCs) and neutrophils that actively produce IL-10. However, M-MDSCs were the cells that sustained the production of IL-10 over the time of infection evaluated. Using mice unable to produce IL-10 (IL-10-/-), we observed that the production of this cytokine during the infection caused by KP35 is important to control bacterial burden, to prevent lung damage, to modulate cytokine production, and to improve host survival. Importantly, intranasal transfer of bone marrow-derived M-MDSCs from mice able to produce IL-10 at 1 day prior to infection improved the ability of IL-10-/- mice to clear KP35 in the lungs, decreasing their mortality. Altogether, our data demonstrate that IL-10 produced by M-MDSCs is required for bacterial clearance, reduction of lung tissue damage, and host survival during KP35 pneumonia.