Fig. 3.

Potential mechanisms of cytokine storm and secondary pathogen infections resulting from lung microbiota dysbiosis in patients with COVID-19. SARS-CoV-2 infection disrupts lung microbiota eubiosis. Increased abundance of opportunistic pathogens may intensify lung cytokine storm and cause secondary pathogen infections in patients with COVID-19. Pathogen-associated molecular patterns (PAMPs) released from invading opportunistic pathogens may be recognized by host innate lymphocytes such as macrophages and dendritic cells (DCs) via pattern recognition receptors (PRR) including Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and NOD-like receptors (NLRs). These induce expression of proinflammatory factors via NF-κB signaling, interferons via IRF3 signaling, and numerous interferon-stimulated genes (ISGs) via JAK/STAT signaling. Excess cytokines may exacerbate COVID-19 symptoms