Publications by authors named "Laura Esparcia"
Increased recruitment of transitional and non-classical monocytes in the lung during SARS-CoV-2 infection is associated with COVID-19 severity. However, whether specific innate sensors mediate the activation or differentiation of monocytes in response to different SARS-CoV-2 proteins remain poorly characterized. Here, we show that SARS-CoV-2 Spike 1 but not nucleoprotein induce differentiation of monocytes into transitional or non-classical subsets from both peripheral blood and COVID-19 bronchoalveolar lavage samples in a NFκB-dependent manner, but this process does not require inflammasome activation.
View Article and Find Full Text PDFCOVID-19 has overloaded national health services worldwide. Thus, early identification of patients at risk of poor outcomes is critical. Our objective was to analyse SARS-CoV-2 RNA detection in serum as a severity biomarker in COVID-19.
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- SARS-CoV-2 triggers a strong immune response, which is crucial in determining how severe COVID-19 becomes in patients.
- Analysis of blood samples from 276 patients showed that severe cases were linked to a drop in key immune cells (T, B, and NK cells) and changes in specific immune cell types.
- The study highlights the association between severity and a weakened humoral immune response, with implications for developing new treatment strategies for COVID-19.
Background: Patients with coronavirus disaese 2019 (COVID-19) can develop a cytokine release syndrome that eventually leads to acute respiratory distress syndrome requiring invasive mechanical ventilation (IMV). Because IL-6 is a relevant cytokine in acute respiratory distress syndrome, the blockade of its receptor with tocilizumab (TCZ) could reduce mortality and/or morbidity in severe COVID-19.
Objective: We sought to determine whether baseline IL-6 serum levels can predict the need for IMV and the response to TCZ.
Article Synopsis
- SARS-CoV-2 causes COVID-19, which can range from mild symptoms to severe acute respiratory distress syndrome (ARDS) characterized by inflammation and immune dysregulation in patients.
- The study investigates specific immune cell subsets, including dendritic cells and monocytes, in COVID-19 patients of varying severity, comparing them to healthy individuals.
- Findings reveal that certain inflammatory monocytes and dendritic cells, particularly CD1c+ types, are more prevalent in the lungs of severe COVID-19 patients, contributing to a better understanding of the disease mechanism and potential treatments.
The SARS-CoV-2 is responsible for the pandemic COVID-19 in infected individuals, who can either exhibit mild symptoms or progress towards a life-threatening acute respiratory distress syndrome (ARDS). It is known that exacerbated inflammation and dysregulated immune responses involving T and myeloid cells occur in COVID-19 patients with severe clinical progression. However, the differential contribution of specific subsets of dendritic cells and monocytes to ARDS is still poorly understood.
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