MDC/CCL22 depletion in COVID-19 and post-COVID

Abstract

In this article, we explore the role of macrophage-derived chemokine (MDC/CCL22) in COVID-19 immunity. The study included plasma samples of 289 patients with PCR-verified COVID-19 from specialized hospitals. The blood samples were collected at admission, approximately 7 days after the start of infection. Genetic testing of the virus was performed in nasopharyngeal swabs to determine the viral strain for each patient. We also included blood plasma of 69 convalescent patients who had recovered from COVID-19 more than a month prior to the study. Additionally, 51 healthy donors were included in the study as controls. The concentrations of MDC/CCL22 and other cytokines and chemokines were measured with multiplex analysis using Luminex MagPix Technology. The results showed that COVID-19 patients had significantly lower MDC levels in their plasma, regardless of the SARS-CoV-2 strain, compared to healthy donors. This finding suggests that MDC/CCL22 depletion may play a role in COVID-19 immunity. Furthermore, convalescent patients still showed decreased concentrations of MDC/CCL22 more than a month after infection, indicating that this depletion may persist even after recovery. We propose two mechanisms that can explain the reasons leading to MDC/CCL22 depletion. The first is binding and inactivation of this chemokine with SARS-CoV-2 peptides, making it not only undetectable for commercial kits, but also less functionally active. Another mechanism is the dysfunction of its effector cells (e.g., DCs and macrophages). Lymphopenia following COVID-19 can potentially be explained by the absence of MDC/CCL22. This may lead to a shift towards hyperactivation in the inflammatory response, potentially explaining the severity of COVID-19. This research sheds light on the importance of MDC/CCL22 in COVID-19 immunity and highlights the need for further investigation into its role in the disease. Understanding the mechanisms behind MDC/CCL22 depletion could provide new insights into the pathogenesis of COVID-19 and inform the development of potential treatments.