Study offers new insights on COVID-19 inflammation
Different markers in the blood clearly differentiate excessive inflammation in critical novel coronavirus (COVID-19) from cytokine storm syndromes, according to a new study published in the journal Arthritis & Rheumatology.
Severe cases of COVID-19 can involve extensive inflammation in the body, and clinicians have wondered if this state is similar to what are called cytokine storm syndromes, in which the immune system produces too many inflammatory signals that can sometimes lead to organ failure and death.
For the study, researchers from the at University Children's Hospital Muenster in Germany quantified levels of 22 biomarkers in serum samples of COVID‐19, including healthy controls, using bead array assay as well as single‐marker ELISA and correlated results with disease outcome.
According to the study, the researchers observed dramatic activation of the interleukin (IL)‐18‐interferon (IFN)‐γ axis, while increased serum levels of IL‐1 receptor antagonist (IL‐1Ra), intracellular adhesion molecule 1 (ICAM‐1), and IL‐8, as well as strongly reduced levels of soluble Fas ligand (sFasL) in course of SARS‐CoV‐2 infection discriminate immune dysregulation in critical COVID‐19 from the investigated well‐recognized cytokine storm conditions.
Serum biomarker profiles clearly separate COVID‐19 from MAS or sHLH, which questions the significance of systemic hyperinflammation following SARS‐CoV‐2 infection as well as the efficacy of drugs targeting key molecules and pathways specifically associated with systemic cytokine storm conditions in the treatment of COVID‐19, the researchers said.
"When we first became aware of a possible association of particularly critical COVID-19 with cytokine storm,” said Christoph Kessel, PhD, lead author of the study, in a statement, “this was intriguing for us, as in the field of autoinflammation we are treating and investigating such conditions on a regular basis.”
The research, which was led by investigators at University Children's Hospital Muenster in Germany, could be useful when deciding which treatments to use in different patients. For example, targeting some key molecules and pathways associated with cytokine storm syndromes may not be effective for treating patients with COVID-19.
"Our present research delivers broad insights on the nature and significance of systemic hyperinflammation following SARS-COV-2 infection," Richard Vollenberg, MD, study co-lead author in a statement. "We consider this relevant as we still lack proper angles of attack to treat critically ill patients."
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