Eosinophils as potential biomarkers in respiratory viral infections

Abstract

Eosinophils are bone marrow-derived granulocytes that, under homeostatic conditions, account for as much as 1-3% of peripheral blood leukocytes. During inflammation, eosinophils can rapidly expand and infiltrate inflamed tissues, guided by cytokines and alarmins (such as IL-33), adhesion molecules and chemokines. Eosinophils play a prominent role in allergic asthma and parasitic infections. Nonetheless, they participate in the immune response against respiratory viruses such as respiratory syncytial virus and influenza. Notably, respiratory viruses are associated with asthma exacerbation. Eosinophils release several molecules endowed with antiviral activity, including cationic proteins, RNases and reactive oxygen and nitrogen species. On the other hand, eosinophils release several cytokines involved in homeostasis maintenance and Th2-related inflammation. In the context of SARS-CoV-2 infection, emerging evidence indicates that eosinophils can represent possible blood-based biomarkers for diagnosis, prognosis, and severity prediction of disease. In particular, eosinopenia seems to be an indicator of severity among patients with COVID-19, whereas an increased eosinophil count is associated with a better prognosis, including a lower incidence of complications and mortality. In the present review, we provide an overview of the role and plasticity of eosinophils focusing on various respiratory viral infections and in the context of viral and allergic disease comorbidities. We will discuss the potential utility of eosinophils as prognostic/predictive immune biomarkers in emerging respiratory viral diseases, particularly COVID-19. Finally, we will revisit some of the relevant methods and tools that have contributed to the advances in the dissection of various eosinophil subsets in different pathological settings for future biomarker definition.

Dimethyl fumarate alleviates allergic asthma by strengthening the Nrf2 signaling pathway in regulatory T cells

“…Recruitment of eosinophils further activates the Th2-type allergic immune responses by secreting IL13 ( 32 , 33 ), consequently exacerbating allergic asthma ( 34 ). Thus, the regulation of pro-inflammatory cytokines is vital in restricting asthma and reducing eosinophil infiltration, and pro-inflammatory genes are prognostic indicators of allergies and asthma ( 35 , 36 ). Inhibition of type 2 inflammation to treat allergic asthma has shown effects in clinical trials ( 37 ).…”

ANCOC Score to Predict Mortality in Different SARS-CoV-2 Variants and Vaccination Status

“…Indeed, eosinophils are able to produce substances with direct antiviral activity in their granules, such as eosinophil cationic protein (with ribonuclease activity), and they stimulate the antiviral immune response by acting as an antigen-presenting cell (APC) and enhancing the CD8+ T cell response (which is involved in antiviral immunity). In addition, eosinophils are able to express some Toll-like receptors (TLR) that are important for virus recognition, such as TLR-7, which binds to single-stranded RNA chains and recognizes single-stranded RNA (ssRNA) [ 24 ]. This receptor–ligand binding leads to an increase in adhesion molecules in eosinophils that decrease in peripheral blood and increase in tissues.…”

“…This receptor–ligand binding leads to an increase in adhesion molecules in eosinophils that decrease in peripheral blood and increase in tissues. In the lung, eosinophils can cause a significant inflammatory response through the production of superoxide anions and may be partially responsible for triggering an excessive immune response [ 24 ]. In COVID-19 patients, this mechanism may explain the correlation between eosinopenia and the cytokine storm that occurred in patients with extensive lung involvement and severe disease [ 25 ].…”

Apoptosis and turnover disruption of olfactory sensory neurons in eosinophilic chronic rhinosinusitis

“…EOSs and Th2 cytokines can reduce ACE2 and TMPRSS2 mRNA expression and inhibit SARS-CoV-2 variants, which may decrease the risk of ECRS patients for COVID-19 and an uncontrolled inflammatory response. This means a decreased risk for ongoing OM injury, olfactory function damage, and virus entry into the OB and central nervous system ( Marin et al, 2021 ; Macchia et al, 2023 ). On the contrary, ACE2 and TMPRSS2 gene expressions are upregulated by Th1 cytokines such as interferon-γ and tumor necrosis factor α (TNF-α), increasing the susceptibilities of nECRS patients to COVID-19 and further inflammation in OM and OD ( Chen et al, 2020 ; Kawasumi et al, 2022 ).…”