The balance between T-helper 1 (Th1) and T-helper 2 (Th2) cells plays an important role in the pathogenesis of brucellosis. Interleukin (IL)-33 induces the activation of Th2 cells while soluble suppression of tumorigenicity 2 (sST2) is a decoy receptor to antagonize the effect of IL-33. Herein, we aimed to identify whether plasma IL-33/sST2 levels could reflect the state of brucellosis and help to monitor the treatment. A total of 78 patients were recruited and divided into acute, subacute, and chronic groups. The chronic group was further divided into chronic active brucellosis and chronic stable brucellosis according to the clinical manifestation. Twenty-six volunteers were assigned to the healthy control (HC) group. Plasma IL-33/sST2 levels were detected by enzyme linked immunosorbent assay (ELISA) and other routine laboratory parameters were obtained from the clinical central laboratory. The level of IL-33 in acute (49.48 ± 18.92), subacute (41.35 ± 17.12), chronic active (44.99 ± 16.80), and the chronic stable (28.92 ± 13.12) groups were higher than that in the HC group (11.66 ± 3.26) (p < 0.001). The IL-33 level in the acute group decreased significantly after treatment (49.48 ± 18.92 vs. 29.89 ± 12.92) (p < 0.001). Furthermore, the IL-33 level in the chronic active group (44.99 ± 16.80) was higher than that in the chronic stable group (28.92 ± 13.12) (p < 0.01). Interestingly, IL-33 correlated with white blood cells (WBC) (r = 0.268, p < 0.05) and C-reactive protein (CRP) (r = 0.272, p < 0.05). The level of sST2 increased in the acute (3,717.76 ± 2,036.25), subacute (3,130.41 ± 1,931.71), chronic active (3,381.43 ± 1,394.83), and the chronic stable group (2,707.03 ± 1,260.26) groups compared with the HC group (297.76 ± 290.93) (p < 0.001). However, the sST2 plasma level showed no differences among the groups and did not significantly change after treatment in the acute group. IL-33 can reflect the state of brucellosis and may be a potential biomarker for diagnosis and monitoring treatment for brucellosis.