Contact lens wear is associated with the appearance of plasmin in the tear fluid — preliminary results

Tervo, Timo; Setten, G.‐B. van; Andersson, Rani-Henrik; Salonen, Eeva‐Marjatta; Vaheri, Antti; Immonen, Ilkka; Tarkkanen, Ahti

doi:10.1007/bf02169824

Cited by 23 publications

(5 citation statements)

References 17 publications

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“…The serine protease inhibitor aprotinin has been shown to aid significantly in the healing of injured rabbit corneas, and the presence of cystatins in tear fluid suggests that they also have a role in the protection of the cornea against excessive proteolysis 42,43 . In tear fluid, increased levels of plasmin activity and/or other proteases have been detected in a variety of ocular conditions, including chemical corrosions, viral keratitis, ulceration of corneal grafts, type I acute hypersensitivity reactions, keratoconjunctivitis sicca (dry eye), as well as with the use of contact lenses 44,45 . In Cstbdeficient mice, the lack of the protease inhibitor in tear fluid could result in unusually high endogenous protease activity and subsequent corneal pathology.…”

Section: Discussionmentioning

confidence: 99%

Progressive ataxia, myoclonic epilepsy and cerebellar apoptosis in cystatin B-deficient mice

et al. 1998

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Loss-of-function mutations in the gene (CSTB) encoding human cystatin B, a widely expressed cysteine protease inhibitor, are responsible for a severe neurological disorder known as Unverricht-Lundborg disease (EPM1). The primary cellular events and mechanisms underlying the disease are unknown. We found that mice lacking cystatin B develop myoclonic seizures and ataxia, similar to symptoms seen in the human disease. The principal cytopathology appears to be a loss of cerebellar granule cells, which frequently display condensed nuclei, fragmented DNA and other cellular changes characteristic of apoptosis. This mouse model of EPM1 provides evidence that cystatin B, a non-caspase cysteine protease inhibitor, has a role in preventing cerebellar apoptosis.

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Section: Discussionmentioning

confidence: 99%

Progressive ataxia, myoclonic epilepsy and cerebellar apoptosis in cystatin B-deficient mice

et al. 1998

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“…However, the association between CL-bound proteolytic activity was not restricted to the growth of Staph.aureus on the CL surface. As shown by aerlier studies (Tervo et al 1989a;van Setten et al 1989b), occurence of plasmin in TF seems to be a rather general change during CL wear. Mechanical irritation, allergic reactions and the presence of microbes on the ocular surface (Tervo et al 1989a, van Setten et al 1989dTervo and van Setten 1989) have been proposed to lie behind the CL wear associated plasmin elevation in tears.…”

Section: Discussionmentioning

confidence: 84%

“…It has also been suggested that this coating protects the bacteria against antibiotics . In addition to the risk of bacterial contamination, CLW is also associated with an increase in tear fluid (TF) proteolytic activity (Tervo et al 1989a;van Setten et al 198913). The presence of proteolytic enzymes such as plasmin on the ocular surface during CLW probably augments the risk of bacterial penetration into the corneal stroma (Tervo & van Setten 1989).…”

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confidence: 99%

On the proteolytic activity of contact lenses and bacteria

Joutsimo

Setten

Renkonen

et al. 1990

Acta Ophthalmologica

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Contact lens wear (CLW) has been shown to cause an elevation in tear fluid (TF) plasmin levels. This study investigated whether the proteolytic activity assayed by a caseinolytic technique was also bound by CLs and whether certain bacterial species contribute to the production of plasmin. CLs worn by patients with corneal disease showed proteolytic activity in five out of nine cases when examined on casein agar. Histological and electron microscopic examination of the lenses revealed bacterial adherence and growth on both surfaces of the CLs. Strains of Staph. epidermidis, Staph. aureus, Pseudomonas aeruginosa and Branhamella catarrhalis, isolated from eyes with external infections, were cultured on a modified milk casein agar and examined for their proteolytic activity. Neither cultures of Branhamella catarrhalis nor Staph. aureus showed proteolytic activity when examined by direct caseinolytic assay. The proteolytic activity shown by Staph. epidermidis or Pseudomonas aeruginosa was not affected by a proteinase inhibitor aprotinin. However, when exogenous plasminogen was added into the casein agar, Staph. aureus was shown to produce caseinolytic activity. This activity was interpreted to be due to plasminogen activator (PA) activity. It was inhibited by aprotinin. Examination of culture fluids of the bacterial species mentioned above did not show caseinolytic activity. Culture fluid of Staph. aureus contained PA activity. The present study confirms the ability of certain bacterial species to adhere to CLs. Moreover, proteases such as plasmin and bacterial enzymes are present in TF during CL wear and may even adhere to the surface of CLs. Hence, bacterial growth probably contributes to the production of proteases on the ocular surface during CL wear.

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“…Such use of CLs could deserve more attention in the treatment of DEDs than currently applied [75]. CL wear itself, in turn, is known to increase enzymatic activity at the surface such that as of plasmin [133]. As plasmin can degrade HA, it can break down HMW molecules to small size molecules, changing the characteristics of topical HA from anti-inflammatory friend to a pro-inflammatory foe.…”

Section: Reducing the Impact Of Attrition: Dry Eye Therapymentioning

confidence: 99%

Impact of Attrition, Intercellular Shear in Dry Eye Disease: When Cells are Challenged and Neurons are Triggered

Setten

2020

IJMS

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The mechanical component in the pathophysiology of dry eye disease (DED) deserves attention as an important factor. The lubrication deficit induced impaired mechano-transduction of lid pressure to the ocular surfaces may lead to the dysregulation of homeostasis in the epithelium, with sensations of pain and secondary inflammation. Ocular pain is possibly the first sign of attrition and may occur in the absence of visible epithelial damage. Attrition is a process which involves the constant or repeated challenge of ocular surface tissues by mechanical shear forces; it is enhanced by the thinning of corneal epithelium in severe DED. As a highly dynamic process leading to pain and neurogenic inflammation, the identification of the impact of attrition and its potential pathogenic role could add a new perspective to the current more tear film-oriented models of ocular surface disease. Treatment of DED addressing lubrication deficiencies and inflammation should also consider the decrease of attrition in order to stimulate epithelial recovery and neural regeneration. The importance of hyaluronic acid, its molecular characteristics, the extracellular matrix and autoregulative mechanisms in this process is outlined. The identification of the attrition and recognition of its impact in dry eye pathophysiology could contribute to a better understanding of the disease and optimized treatment regimens.

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Contact lens wear is associated with the appearance of plasmin in the tear fluid — preliminary results

Cited by 23 publications

References 17 publications

Progressive ataxia, myoclonic epilepsy and cerebellar apoptosis in cystatin B-deficient mice

Progressive ataxia, myoclonic epilepsy and cerebellar apoptosis in cystatin B-deficient mice

On the proteolytic activity of contact lenses and bacteria

Impact of Attrition, Intercellular Shear in Dry Eye Disease: When Cells are Challenged and Neurons are Triggered

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