Objective: To elucidate the mechanism of strong inflammatory response in severe acute respiratory syndrome (SARS) patients.
Methods: 24 patients managed with a standard corticosteroid protocol developed by Peking Union Medical College Hospital were followed up for 2 months and their clinical outcomes were documented. Plasma levels of interleukin (IL)-1 beta, IL-2, IL-4, IL-8, IL-10, IL-12 p70, interferon gamma (IFN gamma), and tumor necrosis factor alpha (TNF alpha) were determined by quantitative ELISA during the course of disease respectively. 12 healthy blood donors were used as normal controls.
Results: All SARS patients had remarkably increased plasma IL-8 concentrations (median 31.23 ng/L) at the onset of disease compared with those of normal controls (6.28 ng/L, P < 0.01). Along with the course of disease IL-8 concentration kept going up and 75% (18/24) patients reached a peak median concentration of 149.65 ng/L (P < 0.01) at the third and fourth weeks. IL-8 came back to normal control levels one month after discharged from hospital. Meanwhile, SARS patients also showed high a TNF alpha level (median 23.12 ng/L) (P < 0.01) at the second week and reached a peak median of 136.35 ng/L (P < 0.05) at the third an fourth weeks. One month after discharged from hospital the plasma TNF alpha concentration fell down to a median of 94.88 ng/L, but it was still much higher than normal controls (3.77 ng/L, P < 0.01).
Conclusion: The SARS-associated coronovirus infection may cause complex cytokine cascade. IL-8 and TNF alpha probably play important roles in mediating strong inflammatory response, which are thought to be responsible for lung injury in SARS patients.