Immunity and inflammatory biomarkers in COVID‐19: A systematic review

Abstract

Coronavirus disease 2019 (COVID-19) is a clinical syndrome caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus. Patients can be asymptomatic or present respiratory and gastrointestinal symptoms, and even multiple-organ failure which can lead to death. The balance between an effective antiviral response and dysregulated immune response is the key factor determining the severity of COVID-19 progression. A systematic review was performed using the NCBI-PubMed database to find the articles related to COVID-19 immunity and inflammatory response published from 1 December 2019 to 15 April 2020. Haematological, immunological and biochemical parameters were extracted and correlated with disease severity, age and presence of comorbidities. Twelve articles were analysed comprising a total of 1042 hospitalized patients infected with SARS-CoV-2 and 95 different parameters. Total lymphocyte count and levels of CD3+ and CD4+ T cells were decreased in severe and critical cases. Neutrophilia was found in patients who progressed to acute respiratory distress syndrome (ARDS). Interleukin-six (IL-6) was high in mild and severe patients regardless of comorbidities.Erythrocyte sedimentation rate (ESR) and count and C-reactive protein (CRP) levels were increased regardless of disease severity or presence of comorbidities. High levels of D-dimer and lactate dehydrogenase were present in diabetic patients and patients who developed ARDS. Procalcitonin levels were elevated to varying degrees in severe and critical patients. We conclude that the total lymphocyte count, CD3+ and CD4+ T cells are low, especially in severe and critical COVID-19 patients; ESR, CRP and IL-6 were elevated, independent of the severity of disease.Understanding the inflammatory response of COVID-19 patients is essential for the development of better therapeutic and management strategies.

Identification of Parameters Representative of Immune Dysfunction in Patients with Severe and Fatal COVID-19 Infection: a Systematic Review and Meta-analysis

“…Other inflammatory parameters, including WBC, PCT, ESR, and SAA, were also proposed as the predictors of fatality. Our synthesis agrees with the findings of previous studies [179][180][181][182][183]. All patients with COVID-19, regardless of the severity, should be screened for hyperinflammation as precaution for potential ARDS once increases in these indicators are detected.…”

SARS-CoV-2 Infection and Lung Regeneration

“…Aberrant activation of macrophages and neutrophils has been observed in patients with severe COVID-19 and contributes to the development of acute respiratory distress syndrome (ARDS) ( 101 – 103 ). The T-cell count was low, especially in severe COVID-19 patients ( 104 ). As evidence accumulates, it is becoming clear that longer hospitalization and higher incidence of critical disease are related to reduced and delayed neutralizing antibody response or production of IFN-λ and type I IFN, along with the rampant production of pro-inflammatory cytokines, such as TNF, IL-6, and IL-8 ( 105 – 109 ).…”

Mesenchymal stem cells and their derived exosomes to combat Covid–19

“… 31 , 32 , 33 , 34 , 35 During infection, neutrophils, monocytes, and T cells are recruited to the site of infection by following the chemoattractant gradient of inflammatory chemokines and chemokines produced by infected cells. 36 Under severe conditions, lymphocyte and leukocyte counts decrease, whereas inflammation marker (C‐reactive protein), lactic dehydrogenase, proinflammatory cytokines and chemokines (interleukin (IL) 1β, IL‐6, IL‐7, IL‐2, tumor necrosis factor (TNF)α, granulocyte‐colony stimulating factor (GCSF), interferon gamma‐induced protein‐10 (CXCL10), and monocyte chemoattractant protein‐1) are elevated dramatically. 37 , 38 , 39 The production of large amounts of proinflammatory cytokines by inflammatory cells leads to cytokine storm resulting in hyperinflammation and subsequently serious lung damage.…”

“…For instance, inflammatory factors in the host body modify the properties of MSCs to modulate the immune system. 25 , 36 The release of inflammatory mediators in the lung is regulated by the differential activation of damage‐associated molecular patterns (DAMPs) presented on the MSCs surface. Toll‐like receptors (TLRs) are activated by viral RNA (TLR3) and viral unmethylated CpG‐DNA (TLR9) leading to substantial cellular signaling pathways and activation of MSCs.…”