Do iL-1 and IL-23 mediate early IL-17A production in pulmonary inflammation leading to late fibrosis?
Our findings demonstrate the existence of an early IL-1β-IL-23-IL-17A axis leading to pulmonary inflammation and fibrosis and identify innate IL-23 and IL-17A as interesting drug targets for IL-1β driven lung pathology.
The results show a higher oxygenation potential of HBOC than with autologous stored red cells because of a more pronounced oxygen extraction.