Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection would stimulate human immune system, trigger the activation and aggregation of various immune cells, and lead to the secretion of a large number of chemokines and cytokines, including interleukin 6 (IL-6), IL-10, granulocyte colony-stimulating factor (G-CSF), interferon γ (IFN-γ), tumor necrosis factor γ (TNF-γ), C-C motif chemokine ligand 2 (CCL2), C-X-C motif chemokine ligand 10 (CXCL10) and other cytokines. The development of uncontrolled systemic inflammatory response is a key factor in patients with critical COVID-19. Mild patients have milder inflammation and mild symptoms, but the lung inflammation in critical ones is more severe: the inflammatory factor expression levels are abnormally high; the infiltration of lung inflammatory cells is obvious along with the histopathological changes of viral pneumonia and inflammatory pneumonia. Continuous immunity response causes the accumulation of lung fibrin, permeability change, injury of the pulmonary blood vessels, and ultimately destroys the lung structure and affects ventilation and circulatory function of the lung. Therefore, continuous and severe inflammation is closely related to acute respiratory distress syndrome, multiple organ dysfunction syndrome, and disseminated intravascular coagulation in critical COVID-19 patients, which is the key point for the transition from mild to critical patients.