Host immune responses play a key role in
COVID-19 pathogenesis. The underlying phenomena are orchestrated by signaling molecules such as
cytokines/
chemokines and
lipid mediators. These immune molecules, including anti-SARS-CoV-2
antibodies, interact with immune cells and regulate host responses, contributing to
inflammation that drives the disease. We investigated 48 plasma
cytokines/
chemokines, 21
lipid mediators, and anti-S
protein (RBD)
antibodies in
COVID-19 patients (n = 56) and non-COVID-19 respiratory disease controls (n = 49), to identify immune-
biomarker profiles.
Cytokines/
chemokines (IL-6, CXCL-10 (IP-10), HGF, MIG, MCP-1, and
G-CSF) and
lipid mediators (TxB2, 11-
HETE, 9-HODE, 13-HODE, 5-
HETE, 12-
HETE, 15-
HETE, 14S-HDHA, 17S-HDHA, and 5-oxo ETE) were significantly elevated in
COVID-19 patients compared to controls. In patients exhibiting severe disease, pro-inflammatory
cytokines/
chemokines (IL-6, CXCL-10, and HGF) and anti-SARS-CoV-2
antibodies were significantly elevated. In contrast,
lipid mediators involved in the reduction/resolution of
inflammation, in particular,
5-HETE,
11-HETE, and
5-oxoETE, were significantly elevated in mild/moderate disease. Taken together, these immune-
biomarker profiles provide insight into immune responses related to
COVID-19 pathogenesis. Importantly, our findings suggest that elevation in plasma concentrations of
IL-6, CXCL-10, HGF, and anti-SARS-CoV-2
antibodies can predict severe disease, whereas elevation in
lipid mediators peaks early (compared to
cytokines) and includes induction of mechanisms leading to reduction of
inflammation, associated complications, and maintenance of homeostasis.