Research Article Quiescent and Active Tear Protein Profiles to Predict Vernal Keratoconjunctivitis Reactivation Alessandra Micera, 1 Antonio Di Zazzo, 1 Graziana Esposito, 1 Roberto Sgrulletta, 2 Virginia L. Calder, 3 and Stefano Bonini 2 1 IRCCS-G.B. Bietti Foundation, 00100 Rome, Italy 2 Department of Ophthalmology, Campus Bio-Medico University, 00128 Rome, Italy 3 UCL Institute of Ophthalmology, London EC1V 9EL, UK Correspondence should be addressed to Stefano Bonini; s.bonini@unicampus.it Received 16 November 2015; Accepted 17 January 2016 Academic Editor: Sung-Hoon Kim Copyright © 2016 Alessandra Micera et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. Vernal keratoconjunctivitis (VKC) is a chronic recurrent bilateral infammation of the conjunctiva associated with atopy. Several infammatory and tissue remodeling factors contribute to VKC disease. Te aim is to provide a chip-based protein analysis in tears from patients sufering from quiescent or active VKC. Methods. Tis study cohort included 16 consecutive patients with VKC and 10 controls. Participants were subjected to clinical assessment of ocular surface and tear sampling. Total protein quantifcation, total protein sketch, and protein array (sixty protein candidates) were evaluated. Results. An overall increased Fluorescent Intensity expression was observed in VKC arrays. Particularly, IL1, IL15, IL21, Eotaxin2, TACE, MIP1, MIP3, NCAM1, ICAM2, NGF, NT4, BDNF, FGF, SCF, MMP1, and MMP2 were increased in quiescent VKC. Of those candidates, only IL1, IL15, IL21, NGF, SCF, MMP2, Eotaxin2, TACE, MIP1, MIP3, NCAM1, and ICAM2 were increased in both active and quiescent VKC. Finally, NT4, FGF, and MMP1 were highly increased in active VKC. Conclusion. A distinct “protein tear-print” characterizes VKC activity, confrming some previously reported factors and highlighting some new candidates common to quiescent and active states. Tose candidates expressed in quiescent VKC might be considered as predictive indicators of VKC reactivation and/or exacerbation out- of-season. 1. Introduction Vernal keratoconjunctivitis (VKC) is a multifactorial eye disease associated with atopy, characterized by a chronic recurrent bilateral infammation of the conjunctiva [1]. Tis childhood disease resolves spontaneously at puberty, although complications might occur due to severe and/or long-standing infammation, leading to fbrovascular reac- tion, new collagen deposition, huge tissue remodeling, and permanent visual changes [2]. Recurrent local infammation might also trigger corneal impairment as well as undesired corneal ulcers [2]. A late onset VKC-like disease has been also observed in young adults with signs/symptoms resembling the childhood disease and characterized by minor corneal involvement [3]. VKC infammation is variable (mild, moder- ate, or severe), ranging from seasonal (acute) to chronic, and resembling the perennial seasonal conjunctivitis [2]. Current knowledge indicates that several infammatory and tissue remodeling factors contribute to signs and symp- toms of VKC [4]. Infltrating T2 cells and eosinophils, recruited mast cells and activated fbroblast/myofbroblasts drive the chronic infammatory process by releasing solu- ble mediators, cytokines/chemokines, adhesion molecules, neuropeptides, and growth factors [5–9]. Secreted proteins accumulate in the tear fuid, representing a “tear-print” of the infamed ocular surface and a view to physiopatho- logical status. Increased cytokines belonging to T1 (IFN, IL2) and T2 (IL4, IL5) subgroups have been detected in tears and conjunctival impression cytologies (IC) from VKC patients [7–10]. In addition, chemokines/adhesion molecules, growth/angiogenic/profbrogenic factors, and receptors of innate immunity contribute actively to the local infamma- tion, as observed in both tears and ICs, or provided by in vitro studies [11–13]. Advances in protein analysis have been done Hindawi Publishing Corporation BioMed Research International Volume 2016, Article ID 9672082, 10 pages http://dx.doi.org/10.1155/2016/9672082