Tinnitus is the perception of sound without an external stimulus. Recently, inflammation has been implicated in the pathophysiology of tinnitus. In tinnitus animal models, cytokine levels are increased throughout the whole auditory pathway, and microglia and astrocytes are activated. However, only a few human studies on inflammation in tinnitus were conducted, which generally did not account for confounders such as hearing loss, anxiety and depression. The current study therefore aimed to evaluate the association between inflammation and tinnitus specifically in participants with (near-)normal hearing and without signs of anxiety or depression. In this cross-sectional study, fifty tinnitus participants and fifty healthy controls completed a tinnitus questionnaire and underwent audiometric testing. Complete blood count measures were determined in blood plasma, as well as cytokine concentrations by using the enzyme-linked immunosorbent assay (ELISA) technique. Platelet count and cytokine concentrations of IL-10 and IFN-γ were lower in participants with tinnitus compared to controls, and male sex, lower MCV, lower platelet count, and lower IL-10 and IFN-γ concentrations were significant predictors of tinnitus presence. The current study shows that inflammatory parameters are altered in tinnitus patients after exclusion of important confounders such as hearing loss, anxiety, depression, and inflammatory diseases.