Here we demonstrate through the use of IL-22BP-knockout mice (il-22ra2<sup>-/-</sup>) that a pro-IL-22 environment reduces pulmonary inflammation during H1N1 (PR8/34 H1N1) infection and protects the lung by promoting tight junction formation.
Our studies also show that PIV depletes IL-22 <i>in vivo</i> Moreover, PIV-mediated enhancement of pneumonia and disease severity was dependent on the expression of pneumolysin (Ply), a prominent virulence factor of <i>S. pneumoniae</i> Altogether, we reveal that PIV and Ply additively potentiate pneumonia in a murine model of lung infection.<b>IMPORTANCE</b><i>S. pneumoniae</i> remains the leading cause of bacterial pneumonia despite widespread use of pneumococcal vaccines, forcing the necessity for appropriate treatment to control pneumococcal infections.Coinfections involving <i>S. pneumoniae</i> with other bacterial pathogens threaten antibiotic treatment strategies and disease outcomes.
Thus, the resistance of newborn mice to pneumonia relied on commensal bacteria-directed ILC3 influx into the lungs, which mediated IL-22-dependent host resistance to pneumonia during this developmental window.
Recent data show the involvement in COPD pathophysiology of interleukin (IL)-17 and IL-22, two cytokines that are important in the control of lung inflammation and infection.
This study demonstrated that the IL-22/IL-22BP system plays a major role during Pseudomonas aeruginosa pneumonia by moderating neutrophil accumulation in the lungs that ultimately leads to epithelium protection.
Delayed clearance of the bacteria and stronger lung inflammation observed in infected CS-exposed mice were associated with an altered production of IL-17 and IL-22 by innate immune cells.