Abstract:In December 2019, a novel coronavirus known as SARS-CoV-2 was first detected in Wuhan, China, causing outbreaks of the coronavirus disease COVID-19 that has now spread globally. For this reason, The World Health Organization (WHO) declared COVID-19 a public health emergency in March 2020. People living with pre-existing conditions such as obesity, cardiovascular diseases, type 2 diabetes (T2D), and chronic kidney and lung diseases, are prone to develop severe forms of disease with fatal outcomes. Metabolic dis… Show more
“…The risk for cardiovascular heart disease (CVD) is higher in people with ‘central’ or ‘visceral-abdominal’ obesity [ 8 ]; CVD, especially heart failure, is a significant risk factor for worse outcomes in COVID-19 [ 9 ]. The innate immune response is also altered in diseases, such as obesity and type 2 diabetes mellitus (T2DM), thus making people more susceptible to SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection [ 10 ]. However, a higher BMI is also frequently associated with a worse prognosis and higher mortality in COVID-19 patients [ 11 , 12 ].…”
“…The risk for cardiovascular heart disease (CVD) is higher in people with ‘central’ or ‘visceral-abdominal’ obesity [ 8 ]; CVD, especially heart failure, is a significant risk factor for worse outcomes in COVID-19 [ 9 ]. The innate immune response is also altered in diseases, such as obesity and type 2 diabetes mellitus (T2DM), thus making people more susceptible to SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infection [ 10 ]. However, a higher BMI is also frequently associated with a worse prognosis and higher mortality in COVID-19 patients [ 11 , 12 ].…”
“…Pattern recognition receptors (PRRs) expressed on innate immune cells, such as DCs and macrophages, recognize and bind surface viral epitopes, leading to anti-pathogen responses. The activation of these cells by the virus leads secretion of several inflammatory cytokines and chemokines, which activate and recruit other immune cells generating a positive feedback loop of inflammation ( Pérez-Galarza et al, 2021 ). Aging alters also these actors involved in innate immunity in terms of both number/percentage and functionality, with different quantitative and qualitative consequences for DCs, monocytes, macrophages, neutrophils and myeloid derived suppressor cells (MDSCs) ( Agrawal et al, 2017 ; Ventura et al, 2017 ; Oh et al, 2019 ; Feng et al, 2021 ).…”
Section: Other Cells Of Innate Immunity: Dendritic Cells (Dcs) Monocytes Macrophages Neutrophils and Myeloid Derived Suppressor Cells (Mdmentioning
The outcomes of Coronavirus disease-2019 (COVID-19) vary depending on the age, health status and sex of an individual, ranging from asymptomatic to lethal. From an immunologic viewpoint, the final severe lung damage observed in COVID-19 should be caused by cytokine storm, driven mainly by interleukin-6 and other pro-inflammatory cytokines. However, which immunopathogenic status precedes this “cytokine storm” and why the male older population is more severely affected, are currently unanswered questions. The aging of the immune system, i.e., immunosenescence, closely associated with a low-grade inflammatory status called “inflammageing,” should play a key role. The remodeling of both innate and adaptive immune response observed with aging can partly explain the age gradient in severity and mortality of COVID-19. This review discusses how aging impacts the immune response to the virus, focusing on possible strategies to rejuvenate the immune system with stem cell-based therapies. Indeed, due to immunomodulatory and anti-inflammatory properties, multipotent mesenchymal stem cells (MSCs) are a worth-considering option against COVID-19 adverse outcomes.
“…It leads to the emergence of oligoclonal B cell populations with high serum oligoclonality, and to the presence of autoAb, particularly against coagulation and vessel targets [14,15]. These comorbidities have in common chronic systemic low-grade inflammation, with an abnormal production of pro-inflammatory cytokines and the impairment of T cell mediated immune response involved in host defense [16][17][18][19]. These immune defects affect several critical pathways that support the cooperation between T cells and B cells, such as the CD40/CD40 ligand pathway, which are probably even more deregulated by the inflammation caused by the SARS-CoV-2 infection.…”
Individuals with pre-existing chronic systemic low-grade inflammation are prone to develop severe COVID-19 and stronger anti-SARS-CoV-2 antibody responses. Whether this phenomenon reflects a differential expansion of antiviral B cells or a failure to regulate antibody synthesis remains unknown. Here, we compared the antiviral B cell repertoire of convalescent healthcare personnel to that of hospitalized patients with pre-existing comorbidities. Out of 277,500 immortalized B cell clones, antiviral B cell frequencies were determined by indirect immunofluorescence screening on SARS-CoV-2 infected cells. Surprisingly, frequencies of SARS-CoV-2 specific clones from the two groups were not statistically different, despite higher antibody levels in hospitalized patients. Moreover, functional analyses revealed that several B cell clones from healthcare personnel with low antibody levels had neutralizing properties. This study reveals for the first time a key qualitative defect of antibody synthesis in severe patients and calls for caution regarding estimated protective immunity based only on circulating antiviral antibodies.
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