Introduction
Coronavirus disease 2019 (COVID-19) first appeared in Wuhan, China in December 2019 and rapidly spread worldwide. To date, more than 75 million confirmed cases have been reported, and this number continues to increase daily. The clinical presentation of COVID-19 is often asymptomatic or consists of mild symptoms such as fever, sore throat, loss of taste and smell, fatigue, and/or joint pain. However, it can have a severe course in individuals of advanced age and those who have hypertension, diabetes, HIV, are receiving long-term immunosuppressive drugs, or have impaired immunity for other reasons1,2.
The most common severe clinical presentations are acute respiratory distress syndrome (ARDS) involving hypoxemic respiratory failure, and macrophage activation syndrome (MAS) 3. In both of these clinical conditions, overexpression of proinflammatory cytokines causes endothelial dysfunction and can result in vital organ injury, especially to the lungs. Interleukin-2 (IL-2), IL-6, IL-7, tumor necrosis factor alpha (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) are the main parameters observed at significant levels and associated with prognosis in studies of COVID-19 patients who need intensive care 4,5.
Surfactant protein-A (SP-A), a member of the innate immune system, is in the collectin family of proteins synthesized by type 2 alveolar epithelium. Other members of this family include SP-D and mannose-binding lectin (MBL). These proteins mainly target alveolar macrophages, dendritic cells, and T cells and play an important role in agglutination, opsonization, and modulation. In patients who present with acute respiratory failure, SP-A level gradually increases with number of days on mechanical ventilation, and low initial SP-A level is associated with severe course and poor prognosis 6. Moreover, during the influenza-A pandemic, a single nucleotide polymorphism in SP-A was found to be associated with poor prognosis and clinical course. In noninfectious pulmonary diseases such as lung cancers, SP-A induces the differentiation of monocytes into M1 monocytes and the synthesis of perforin-1 and granzyme-B in natural killer cells, thus exerting an anti-tumoral effect 7.
Considering the previously documented roles of MCP-1 in COVID-19 prognosis and that of SP-A in inflammatory and noninflammatory lung diseases, especially ARDS, the present study was conducted to examine the relationship between these parameters and clinical course and prognosis in COVID-19 patients.