The discovery of DEFB-109 on the ocular surface enhances our knowledge of the profile of AMPs at this important mucosal surface. The fact that its expression is significantly reduced in both inflammatory and infective ocular surface disease reflects not only an intimate balance between this host defense gene and microbes but indicates a role other than purely microbicidal. This discovery will enable the mechanisms behind the intriguing phenomenon of reduced gene expression of an AMP in disease states to be uncovered.

Aim: To investigate the safety and efficacy of alcohol delamination of the corneal epithelium for recalcitrant recurrent corneal erosion syndrome (RCE) in a prospective non-comparative interventional case series. Methods: Patients with RCE who remained symptomatic despite topical lubrication and 3-month use of an extended wear (bandage) contact lens were included. The intensity of pain on a scale of 1 to 10, and duration and frequency of attacks were recorded. Patients were treated with alcohol delamination and followed up at 1 week, 1 month and then at 12 months, which was the minimum follow up time. Success was defined as a resolution of symptoms after 1 month of treatment, and partial success as a significant reduction in symptoms manageable with topical lubricants, and failure where symptoms were unchanged or worsened. Results: 20 eyes of 20 patients with RCE caused by trauma (n = 14), anterior basement membrane dystrophy (n = 5) or idiopathic (1) were studied. The mean age of patients was 44 years and mean follow-up 24 months. Two eyes were lost to follow-up. 15 (83%) eyes were qualified as successes, 3 as partial successes and no failures were seen. No intraoperative complications were observed. 1 patient developed transient subepithelial haze that resolved with topical steroid, 1 had a change in refraction and 1 developed herpetic stromal keratitis 2 months postoperatively, which was successfully treated. No loss of vision was observed in any of the patients. Conclusion: Alcohol delamination of the corneal epithelium is a safe and effective method for treating patients with recalcitrant RCE.

Methods: Human corneal limbal epithelial cells were exposed to AC at different time points, up to 9 hours, the genomic profile of the AMPs were analysed at these time point using real time PCR. HCLE cells not infected with AC were used as controls.Results: Seven of the 8 studied AMPs showed statistically significant upregulation in gene expression. Human beta Defensin 3 (hBD3) showed a very significant 10 fold upregulation in the exposed cells and Ribonuclease-7 (RNase-7) showed a very early and consistent increase. Human beta Defensin 1 (hBD1) was the only downregulated AMP. Conclusions:The study data suggests a possible role of the AMPs in combating the amoebic infection at the ocular surface. Using AMPs singly or in combination is a promising avenue for further exploration in the treatment of the sight threatening Acanthamoeba keratitis.

Antimicrobial peptides are host defence molecules that play a potential role in preventing infection at the epithelial surfaces. Ribonuclease (RNase)-7 has been shown to possess a broad spectrum of microbicidal activity against various pathogens. Here, we demonstrate that RNase-7 protein is localised to the superficial layers of ocular surface cells and increased in response to interleukin (IL)-1β, suggesting an active role during inflammation related to ocular surface infection. Signal transduction pathways involved in RNase-7 expression are unknown. Involvement of transforming growth factor β-activated kinase-1 (TAK-1) activated nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathway molecules [c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and p38] were studied because of their importance in infection and inflammation. Blocking the MAPKs resulted in inhibition of RNase-7 expression in response to IL-1β. However, RNase-7 induction by IL-1β was not affected by inhibiting the NF-κB signalling pathway. In conclusion, our results indicate that RNase-7 expression is specifically mediated via MAPKs but not NF-κB signalling pathways.