•Liver biopsies at stage F1 to F3 expressed more IL-22 than F0 or F4.
•The number of cells expressing IL-22R1 decreased as fibrosis increased.
•There was an increase in Il-22BP staining in more advanced stages of fibrosis.
•IL-22 pathway may be involved in the pathophysiology of liver fibrosis.
Liver fibrosis is the result of an exacerbated wound-healing response associated with chronic liver injury. Interleukin-22 (IL-22) plays a key role in liver disease, through either a protective or an adverse role, depending on the context. The relationship between IL-22 and its receptors IL-22R1 and IL-22BP (soluble inhibitor) in liver fibrosis is unknown. In this study, we assessed the presence and quantity of IL-22, IL-22R1, and IL-22BP–producing cells in liver tissues of patients with chronic hepatitis C.
Methods and results
The number of IL-22–producing cells was significantly higher in stages F1, F2, and F3 when compared to F0 or F4 (p < 0.05). The immunostaining of IL-22R1 decreased as liver fibrosis increased from F1 to F4. On the other hand, the concentration of IL-22BP–producing cells was higher in patients with cirrhosis (F4). Furthermore, the IL-22BP:IL-22 ratio was highest in patients with cirrhosis.
Our results suggest that IL-22, IL-22R1 and IL-22BP may be involved in the mechanisms of liver fibrosis in patients with chronic hepatitis C.