Corneal surface changes in keratoconjunctivitis sicca. Part I: the surface proper. A non-contact photomicrographic in vivo study in the human cornea

Tabery, Helena M.

doi:10.1038/sj.eye.6700401

Cited by 13 publications

(6 citation statements)

References 17 publications

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“…At higher magnification these stained cells are seen as straight-sided, polygonal cells with uptake of dye into the cytoplasm, but more concentrated uptake in the cell nuclei. This staining pattern was demonstrated convincingly by Tabery (1992Tabery ( , 1998Tabery ( , 2003 and is similar to that seen in vitro in cultured human corneal epithelial cells (Feenstra and Tseng 1992a;). Maldonado-Codina (2014) observed that epithelial staining secondary to MPS exposure involved uptake of dye into individual cells and that, generally fluorescein, lissamine green and rose bengal were taken up into the same cells.…”

Section: Rose Bengalsupporting

confidence: 77%

Clinical staining of the ocular surface: Mechanisms and interpretations

Bron

Argüeso

İrkeç

et al. 2015

Progress in Retinal and Eye Research

140

109

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Section: Rose Bengalsupporting

confidence: 77%

Clinical staining of the ocular surface: Mechanisms and interpretations

Bron

Argüeso

İrkeç

et al. 2015

Progress in Retinal and Eye Research

140

109

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“…103 it also fits in with the observations of Tabery, using fluorescein dye instilled at high concentration, that fluorescein is taken up by (or "adheres" to) the same diseased corneal epithelial cells as those stained by rose bengal. 107,109,123 The caveat should be accepted that these observations may be subject to the same interpretation as that offered by argueso et al in relation to rose bengal staining of cultured corneal epithelial cells. 88 Thus, staining under cell culture conditions may reflect the undifferentiated state of the cultured cells.…”

Section: Fluorescein Sodiummentioning

confidence: 76%

“…This staining pattern has been demonstrated convincingly by Tabery (figure 11). [107][108][109] The staining characteristics of rose bengal in the healthy young eye with an intact epithelium are similar to those of fluorescein, as neither dye stains the healthy epithelium. There are exceptions to this which relate to the presence of chance degenerations of the conjunctiva such as pinguecula, or elevated regions such as the caruncle, which will take stain.…”

Section: B Rose Bengal and Lissamine Greenmentioning

confidence: 86%

A Solute Gradient in the Tear Meniscus. I. A Hypothesis to Explain Marx's Line

et al. 2011

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Marx's line is a line of mucosal staining behind the mucocutaneous junction. It can be demonstrated throughout life in all normal lids by staining with lissamine green and related dyes. Of all the body orifices, only the mucosae of the eye and mouth are directly exposed to the atmosphere. In this paper, we suggest that for the eye, this exposure leads to the formation of Marx's line. The tear meniscus thins progressively toward its apex, where it is pinned at the mucocutaneous junction of the lid. It also thins toward the black line, which segregates the meniscus from the tear film after the blink. We predict that, because of the geometry of the tear meniscus, evaporation generates a solute gradient across the meniscus profile in the anteroposterior plane, which peaks at the meniscus apices at the end of the interblink. One outcome would be to amplify the level of tear molarity at these sites so that they reach hyperosmolar proportions. Preliminary mathematical modeling suggests that dilution of this effect by advection and diffusion of solute away from the meniscus apex at the mucocutaneous junction will be restricted by spatial constraints, the presence of tear and surface mucins at this site, and limited fluid flow. We conclude that evaporative water loss from the tear meniscus may result in a physiological zone of hyperosmolar and related stresses to the occlusal conjunctiva, directly behind the mucocutaneous junction. We hypothesize that this stimulates a high epithelial cell turnover at this site, incomplete epithelial maturation, and a failure to express key molecules such as MUC 16 and galectin-3, which, with the tight junctions between surface epithelial cells, are necessary to seal the ocular surface and prevent penetration of dyes and other molecules into the epithelium. This is proposed as the basis for Marx's line. In Part II of this paper (also published in this issue of The Ocular Surface), we address additional pathophysiological consequences of this mechanism, affecting lid margins.

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“…Degree of penetrance of rose bengal, an anionic dye, is an established method of assaying epithelial barrier function [3], [14], [29]. It has previously been demonstrated that corneal epithelial cells exclude this dye [14], and that siRNA knockdown of MUC16 in these cells leads to increased uptake of the dye that in turn is associated with increased pathogen adherence [3].…”

Section: Resultsmentioning

confidence: 99%

A Metalloproteinase Secreted by Streptococcus pneumoniae Removes Membrane Mucin MUC16 from the Epithelial Glycocalyx Barrier

et al. 2012

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The majority of bacterial infections occur across wet-surfaced mucosal epithelia, including those that cover the eye, respiratory tract, gastrointestinal tract and genitourinary tract. The apical surface of all these mucosal epithelia is covered by a heavily glycosylated glycocalyx, a major component of which are membrane-associated mucins (MAMs). MAMs form a barrier that serves as one of the first lines of defense against invading bacteria. While opportunistic bacteria rely on pre-existing defects or wounds to gain entry to epithelia, non opportunistic bacteria, especially the epidemic disease-causing ones, gain access to epithelial cells without evidence of predisposing injury. The molecular mechanisms employed by these non opportunistic pathogens to breach the MAM barrier remain unknown. To test the hypothesis that disease-causing non opportunistic bacteria gain access to the epithelium by removal of MAMs, corneal, conjunctival, and tracheobronchial epithelial cells, cultured to differentiate to express the MAMs, MUCs 1, 4, and 16, were exposed to a non encapsulated, non typeable strain of Streptococcus pneumoniae (SP168), which causes epidemic conjunctivitis. The ability of strain SP168 to induce MAM ectodomain release from epithelia was compared to that of other strains of S. pneumoniae, as well as the opportunistic pathogen Staphylococcus aureus. The experiments reported herein demonstrate that the epidemic disease-causing S. pneumoniae species secretes a metalloproteinase, ZmpC, which selectively induces ectodomain shedding of the MAM MUC16. Furthermore, ZmpC-induced removal of MUC16 from the epithelium leads to loss of the glycocalyx barrier function and enhanced internalization of the bacterium. These data suggest that removal of MAMs by bacterial enzymes may be an important virulence mechanism employed by disease-causing non opportunistic bacteria to gain access to epithelial cells to cause infection.

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Corneal surface changes in keratoconjunctivitis sicca. Part I: the surface proper. A non-contact photomicrographic in vivo study in the human cornea

Cited by 13 publications

References 17 publications

Clinical staining of the ocular surface: Mechanisms and interpretations

Clinical staining of the ocular surface: Mechanisms and interpretations

A Solute Gradient in the Tear Meniscus. I. A Hypothesis to Explain Marx's Line

A Metalloproteinase Secreted by Streptococcus pneumoniae Removes Membrane Mucin MUC16 from the Epithelial Glycocalyx Barrier

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