Jon Roger Eidet1, Øystein Kalsnes Jørstad2, Ida G Fostad3, Ole K Olstad4, Ragnhild Ø Sørland2, Morten C Moe2, Goran Petrovski2, Milaim Pepaj5. 1. Center for Eye Research, Department of Ophthalmology, Oslo University Hospital, University of Oslo, Oslo, Norway. j.r.eidet@gmail.com. 2. Center for Eye Research, Department of Ophthalmology, Oslo University Hospital, University of Oslo, Oslo, Norway. 3. Faculty of Dentistry, Department of Oral Biology, University of Oslo, Oslo, Norway. 4. Blood Cell Research Group, Section for Research, Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway. 5. Hormone Laboratory, Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway.
Abstract
PURPOSE: To determine whether unilateral acute anterior uveitis (AAU) induces ipsilateral changes in the tear fluid proteome. METHODS: Five patients (25-77 years old) with unilateral AAU were included. Tear fluid samples were obtained using Schirmer's test strips. The healthy eye served as control. Proteins were identified by liquid chromatography tandem mass spectrometry. RESULTS: Two hundred forty-two tear fluid sample proteins were identified, of which 75 were present in at least three patients. Nine proteins were at least 1.5-fold increased, whereas eight were at least 1.5-fold decreased in tears from the diseased eye compared with the healthy eye. APOBEC3A was significantly increased (1.43-fold; P = 0.04), whereas TGM2 was significantly decreased (- 1.21-fold; P = 0.03) in tears from the diseased eye relative to the healthy eye. Ingenuity Pathway Analysis identified LXR/RXR (P < 1.02E-4) as a top canonical pathway. CONCLUSION: Unilateral AAU induced detectable changes in the ipsilateral tear fluid proteome and involvement of the inflammation-associated LXR/RXR pathway.
PURPOSE: To determine whether unilateral acute anterior uveitis (AAU) induces ipsilateral changes in the tear fluid proteome. METHODS: Five patients (25-77 years old) with unilateral AAU were included. Tear fluid samples were obtained using Schirmer's test strips. The healthy eye served as control. Proteins were identified by liquid chromatography tandem mass spectrometry. RESULTS: Two hundred forty-two tear fluid sample proteins were identified, of which 75 were present in at least three patients. Nine proteins were at least 1.5-fold increased, whereas eight were at least 1.5-fold decreased in tears from the diseased eye compared with the healthy eye. APOBEC3A was significantly increased (1.43-fold; P = 0.04), whereas TGM2 was significantly decreased (- 1.21-fold; P = 0.03) in tears from the diseased eye relative to the healthy eye. Ingenuity Pathway Analysis identified LXR/RXR (P < 1.02E-4) as a top canonical pathway. CONCLUSION: Unilateral AAU induced detectable changes in the ipsilateral tear fluid proteome and involvement of the inflammation-associated LXR/RXR pathway.