Serum Interleukin-22 in Iraqi Patients with Crohn’s Disease: Association with Biologic Treatment Status and Clinical Disease Activity

Abstract

Background: Interleukin-22 (IL-22) is an immunologically relevant cytokine in Crohn’s disease (CD), but its circulating clinical significance remains uncertain. This study evaluated serum IL-22 in Iraqi patients with CD and examined its association with biologic treatment status and disease activity. Methodology: This case-control study included 120 participants divided into three groups: 30 CD patients receiving biologic therapy, 30 untreated CD patients, and 60 healthy controls. Clinical activity for the patients was assessed using the Harvey–Bradshaw Index (HBI). Serum IL-22 concentrations were compared among the groups together with age and body mass index (BMI). Results: Serum IL-22 levels were significantly elevated in CD patients compared with healthy controls (p = 0.0001). Within the CD cohort, age did not differ significantly between biologically treated and untreated patients (29.33 ± 12.48 vs. 28.70 ± 9.70 years; p = 0.820). In contrast, BMI was significantly higher in the biologic-treatment group (25.44 ± 5.14 vs. 18.52 ± 1.66 kg/m²; p = 0.0001). Patients receiving biologic therapy had markedly lower HBI scores than untreated patients (3.03 ± 1.10 vs. 11.47 ± 3.41; p = 0.0001). Serum IL-22 was also significantly lower in the biologic-treatment group, with median values of 291.38 pg/mL (242.48–367.13) versus 455.36 pg/mL (332.52–562.48) in untreated patients (p = 0.0001.  Conclusion: In this cohort of Iraqi patients with CD, circulating IL-22 levels were significantly higher than in healthy controls. Furthermore, biologic treatment was associated with lower clinical activity and lower circulating IL-22 levels. These findings support a relationship between serum IL-22 and disease state, but they should be interpreted cautiously. Further longitudinal and mechanistic studies are needed to determine whether IL-22 has value as a monitoring biomarker or reflects treatment-modulated inflammatory pathways.