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.