Cytokine Status of Covid-19 Patients

The causative agent of coronavirus 2019 (COVID-19) disease, which started in Wuhan province
of China in December 2019, was severe acute respiratory failure syndrome coronavirus 2
(SARS-CoV-2), which quickly spread all over the world and caused a pandemic. COVID-19 can
cause death with symptoms such as fever, cough, muscle pain, shortness of breath, and
pneumonia (1). Pulmonary pathology of COVID-19 is diffuse alveolar damage, focal reactive
hyperplasia of pneumocytes with patchy inflammatory cells, intravascular thrombosis,
monocyte, macrophage and lymphocyte infiltration into pulmonary spaces. Severe infiltration
of pulmonary tissue affects alveolar gas exchange. In addition, cardiovascular morbidity,
tachyarrhythmia and thromboembolic events are observed in 1/5 of the hospitalized patients
with troponin elevation, which is closely related to mortality. In severe COVID-19
infections, after pulmonary inflammation, cardiovascular organ failure, cytokine storm,
hemophagocytosis, septic shock, develops due to uncontrolled hypoxia, and isolated organ
failure turns into multi-organ failure. It is noteworthy that it causes lymphopenia in
patients. In the studies , the blood levels of certain inflammatory cytokines,
interleukin-1β,interleukin-6 and TNF-α, were evaluated. In addition, blood values of a
limited number of cytokines were investigated in a similar way in a limited number of studies
published in our country.

We aimed to study IL-1β, IFN-α2, IFN-γ, TNF-α, MCP-1 (CCL2), IL-6, IL-8 (CXCL8), IL-10,
IL-12p70, IL-17A, IL-18, IL-23, IL-33 at Covid 19 and healthy volunteers.