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Feature Review | Previous Articles
February 2007


Increased Eotaxin in Tears of Patients Wearing Contact Lenses

Dr Vicki Evans, Head of Clinical Research for the Institute for Eye Research, Australia

Vicki is an optometry graduate from UNSW, Sydney. After working in private practice she conducted clinical trial research on silicone hydrogel lenses with the CCLRU. Vicki completed her PhD in tear film biochemistry and dry eye with the Cooperative Research Centre for Eye Research and Technology in Sydney, Australia and post-doctoral research in the Department of Ophthalmology, Oxford University, UK. From 2002 Vicki was the Professional Affairs Manager for CIBA Vision UK then the Head of Professional Marketing for CIBA Vision Asia Pacific before taking up her current role Head of Clinical Research for the Institute for Eye Research in November 2006.


Review of the paper entitled:

Increased Eotaxin in Tears of Patients Wearing Contact Lenses.  
Marilita M. Moschos, MD, Simone Eperon, PhD, and Yan Guex-Crosier, MD, CORNEA 2004, 23, 8, 771-775

Contact Lens Papillary Conjunctivitis (CLPC) is thought to have a combined mechanical and allergic aetiology, caused by the interaction of the lid with the contact lens surface and the presence of antigenic surface deposits.  The current approach to treating CLPC attempts to remove the mechanical stimuli (change contact lens material, replacement frequency, wear time, ocular lubricants) and treat the allergic inflammatory response (mast cell stabilisers and the new combined anti-allergic/antihistamine compounds).

Allansmith et al (1978) demonstrated that Giant Papillary Conjunctivitis induced by hard or soft contact lens wear could be histologically characterised by the presence of increased inflammatory cells in the tarsal conjunctival tissue.  The papillae contain inflammatory cells, notably eosinophils, mast cells and basophils.

Eosinophils are a type of white blood cell (leucocyte) which play an important role in fighting infection and in allergic inflammatory processes.  Tissue levels of eosinophils typically rise in the event of parasitic infection or allergic reaction.  Eosinophils are lured to the tissue by chemical mediators called chemokines.  One potent attractant for eosinophils is eotaxin, a CC-chemokine, (so called because of the two adjacent cysteine (C) residues on the protein).

The authors hypothesize that detection of eotaxin in tears of contact lens wearers may indicate that an inflammatory eosinophil response is occurring in conjunctival tissue and as such may be marker for CLPC.  If eotaxin is shown to be correlated with the presence or progression of papillae it may have some role (direct or indirect) in the formation of the papillae response in contact lens papillary conjunctivitis (CLPC).  If such a role is shown, then a possible new therapeutic avenue for CLPC may be to investigate eotaxin antagonists.

Interestingly, the authors did not collect tear samples from patients with CLPC, preferring instead to collect samples from a population of successful contact lens wearers.  The authors found increased eotaxin in the tears of contact lens wearers compared to non-wearers and a positive correlation between eotaxin levels and papillae grade in the combined group of wearers and non-wearers.
Leonardi et al, 2003, demonstrated increased eotaxin levels in tears and mucus with allergic conjunctivitis, a finding which may appear to support the author’s hypothesis.  However, Sarac et al, 2003 did not find a role for tear eotaxin, or eotaxin mediated eosinophil recruitment, in ocular prostheses wearers with chronic GPC.  This suggests that the same mechanisms shown to be involved in allergic conjunctivitis by Leonardi et al may not be involved in the development of GPC in ocular prostheses wearers. It also raises the question as to whether the mechanisms involved with CLPC will more closely resemble the allergic conjunctivitis response or the GPC response observed by Sarac et al.

The authors suggest the discrepancy in eotaxin findings between their study and Sarac’s may be due to differences in tear secretion between the study populations and does not rule out a role for eotaxin in CLPC. The authors acknowledge the need for further studies to establish an exact role of eotaxin in the development of papillae associated with contact lens wear and whether it may provide a potential therapeutic approach for CLPC.


  • (search eosinophil and chemokine)
  • Allansmith MR, Korb DR, Greiner JV. Giant papillary conjunctivitis induced by hard or soft contact lens wear: quantitative histology. Ophthalmology 1978 Aug; 85(8):766-78.
  • Leonardi A, Jose PJ, Zhan H, Calder VL. Tear and mucus eotaxin-1 and eotaxin-2 in allergic keratoconjunctivitis. Ophthalmology 2003 Mar; 110(3):487-492.

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