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Aim: To investigate the role of interleukin-17 in ocular surface and corneal disease. Ocular surface and corneal disease is a leading cause of blindness and is an ongoing challenge for the public health sector to implement effective therapies. The majority of cells in corneal lesions are derived primarily from neutrophils that induce inflammatory events that lead to tissue damage. One of the key pro-inflammatory cytokines is IL-17, and it has been investigated in order to facilitate the understanding of the pathogenesis of ocular surface lesion development. Method: A review of the literature was performed through a systematic approach. Results: IL-17 has been shown to exacerbate dry eye disease, viral and bacterial keratitis lesion severity, although it was found to be protective for Acanthamoeba. Antibodies developed to neutralize IL-17 have shown some promise in reducing the severity of some diseases. Conclusion: IL-17 plays a role in the pathogenesis of ocular surface and corneal disease and targeting this cytokine may provide a useful treatment option in the future. [ABSTRACT FROM AUTHOR]

Contact lens wear is a common predisposing factor in microbial keratitis and is one of the two preventable risk factors for corneal infection in a working age population. Our understanding of the prevention and prophylaxis of contact lens-related corneal infection is informed by recent epidemiological studies describing the incidence of and risk factors for the disease, the effect of causative organism on disease severity, and an appreciation of individual immune profiles in susceptibility to and severity of the disease. Although contemporary contact lenses have not reduced the overall incidence of keratitis, a reduction in morbidity may be achievable through recognition of appropriate risk factors in severe disease, including avoiding delays in presenting for appropriate treatment, and attention to storage case hygiene practise. Severe keratitis is most commonly associated with an environmental causative organism, and daily disposable lenses are associated with less severe disease. Pseudomonas aeruginosa remains the commonest cause of contact lens-related corneal infection probably because of its unique virulence characteristics and ability to survive in the contact lens/storage case/ocular environment. In two recent outbreaks of contact lens-related infections, there has been a strong association demonstrated with particular contact lens solutions. Since the recall of these specific contact lens solutions, the rate of Acanthamoeba keratitis has remained above the expected baseline, indicating unidentified risk factors that may include environmental exposures. Individual differences in susceptibility to microbial keratitis may be partly explained by differences in single-nucleotide polymorphisms in certain cytokine genes, particularly those with a proven protective role in corneal infection. [ABSTRACT FROM AUTHOR]

Contact lens wear is a common predisposing factor in microbial keratitis and is one of the two preventable risk factors for corneal infection in a working age population. Our understanding of the prevention and prophylaxis of contact lens-related corneal infection is informed by recent epidemiological studies describing the incidence of and risk factors for the disease, the effect of causative organism on disease severity, and an appreciation of individual immune profiles in susceptibility to and severity of the disease. Although contemporary contact lenses have not reduced the overall incidence of keratitis, a reduction in morbidity may be achievable through recognition of appropriate risk factors in severe disease, including avoiding delays in presenting for appropriate treatment, and attention to storage case hygiene practise. Severe keratitis is most commonly associated with an environmental causative organism, and daily disposable lenses are associated with less severe disease. Pseudomonas aeruginosa remains the commonest cause of contact lens-related corneal infection probably because of its unique virulence characteristics and ability to survive in the contact lens/storage case/ocular environment. In two recent outbreaks of contact lens-related infections, there has been a strong association demonstrated with particular contact lens solutions. Since the recall of these specific contact lens solutions, the rate of Acanthamoeba keratitis has remained above the expected baseline, indicating unidentified risk factors that may include environmental exposures. Individual differences in susceptibility to microbial keratitis may be partly explained by differences in single-nucleotide polymorphisms in certain cytokine genes, particularly those with a proven protective role in corneal infection. [ABSTRACT FROM AUTHOR]

Purpose Autosomal dominant mutations in TGFBI cause a range of clinically distinct corneal dystrophies. We investigated the TGFBI mutation spectrum in our cohort and correlated genotype with phenotype. Methods TGFBI exons 4, 11, 12, 13, 14 and 16 were Sanger sequenced in 59 unrelated probands attending Moorfields Eye Hospital with a diagnosis of a potential TGBFI-associated corneal dystrophy. Results The majority of individuals, 86%, carried a mutation at one of the two known hotspot residues for TGFBI-associated corneal dystrophies: Arg-124 and Arg-555. Mutations affecting either of these residues demonstrated genotype-phenotype correlation. A c.1868G>A; p.(Gly623Asp) mutation was identified in five unrelated probands; one with a clinical diagnosis of lattice corneal dystrophy, two with a Bowman's layer dystrophy (Reis-Bϋcklers or Thiel-Behnke corneal dystrophy) and two with epithelial basement membrane dystrophy (EBMD). The clinical variability associated with this mutation indicates that other genetic or environmental factors can influence phenotypic expression. Conclusions This is the first time the c.1868G>A; p.(Gly623Asp) mutation has been associated with EBMD, although other mutations in TGFBI have previously been identified in a small number of EBMD patients. These results demonstrate that the c.1868G>A; p.(Gly623Asp) mutation is responsible for a significant proportion of the disease burden for TGFBI-associated corneal dystrophies in the UK and highlights the need for patients with EBMD to be screened for mutations in TGFBI. [ABSTRACT FROM AUTHOR]