Expression of growth factors in the conjunctiva from patients with active trachoma

El-Asrar, A M Abu; Al-Kharashi, Soliman A; Missotten, Luc; Geboes, Karel

doi:10.1038/sj.eye.6701884

Cited by 18 publications

(12 citation statements)

References 38 publications

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“…However, abnormal persistent TNC expression is correlated with excessive matrix deposition that leads to collagenous scar formation in several fibrotic diseases [96] – this suggests an equivalent role in chlamydial scarring. Production of a tenascin protein has been previously observed by immunohistochemical studies of conjunctival biopsies taken from patients with trachomatous conjunctivitis [97]. Higher expression is also found in chronic cardiac conditions, and is a reliable indicator of poor patient prognosis [95], [96].…”

Section: Resultsmentioning

confidence: 86%

Simultaneous Transcriptional Profiling of Bacteria and Their Host Cells

et al. 2013

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We developed an RNA-Seq-based method to simultaneously capture prokaryotic and eukaryotic expression profiles of cells infected with intracellular bacteria. As proof of principle, this method was applied to Chlamydia trachomatis-infected epithelial cell monolayers in vitro, successfully obtaining transcriptomes of both C. trachomatis and the host cells at 1 and 24 hours post-infection. Chlamydiae are obligate intracellular bacterial pathogens that cause a range of mammalian diseases. In humans chlamydiae are responsible for the most common sexually transmitted bacterial infections and trachoma (infectious blindness). Disease arises by adverse host inflammatory reactions that induce tissue damage & scarring. However, little is known about the mechanisms underlying these outcomes. Chlamydia are genetically intractable as replication outside of the host cell is not yet possible and there are no practical tools for routine genetic manipulation, making genome-scale approaches critical. The early timeframe of infection is poorly understood and the host transcriptional response to chlamydial infection is not well defined. Our simultaneous RNA-Seq method was applied to a simplified in vitro model of chlamydial infection. We discovered a possible chlamydial strategy for early iron acquisition, putative immune dampening effects of chlamydial infection on the host cell, and present a hypothesis for Chlamydia-induced fibrotic scarring through runaway positive feedback loops. In general, simultaneous RNA-Seq helps to reveal the complex interplay between invading bacterial pathogens and their host mammalian cells and is immediately applicable to any bacteria/host cell interaction.

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Section: Resultsmentioning

confidence: 86%

Simultaneous Transcriptional Profiling of Bacteria and Their Host Cells

et al. 2013

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“…While conjunctiva-derived CTGF has already been described earlier in humans, 11 others failed to detect CTGF in normal human conjunctiva. 27 As also seen for fibrotic processes in other systems, e.g., skin, 27 or kidney, 28 CTGF is also upregulated in the conjunctiva of ocular cicatricial pemphigoid. 11 However, CTGF was not detected in conjunctiva of trachoma patients, 27 and it was found to be decreased in ulcerated eyes in an animal study (most likely due to dilution effects as a result of increased tear production in that case).…”

Section: Discussionmentioning

confidence: 96%

“…27 As also seen for fibrotic processes in other systems, e.g., skin, 27 or kidney, 28 CTGF is also upregulated in the conjunctiva of ocular cicatricial pemphigoid. 11 However, CTGF was not detected in conjunctiva of trachoma patients, 27 and it was found to be decreased in ulcerated eyes in an animal study (most likely due to dilution effects as a result of increased tear production in that case). 7 Summarizing aforementioned reports, two possible actions of conjunctival CTGF are postulated: first via secretion into the tear fluid and second as a mediator into deeper layers of the conjunctiva.…”

Section: Discussionmentioning

confidence: 96%

Immunohistochemical Detection of CTGF in the Human Eye

Setten

Trost

Schrödl

et al. 2016

Current Eye Research

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“…Endoglin, a 70.6 kDa protein is a transmembrane constituent of the transforming growth factor beta receptor complex and in the eye is highly expressed throughout, including cornea and conjunctiva (NEIBank), particularly on vascular endothelial cells of trachoma conjunctiva (Abu El-Asrar et al, 2006), and on corneal mesenchymal stromal cells (Bray et al, 2014) that are considered to have stem-like properties (Hashmani et al, 2013). In choroidal neovascularization secondary to age-related macular degeneration, endothelial expression is increased (Grisanti et al, 2004).…”

Section: Other Autophagy ‘Eye Disease Genes’ Of the Ocular Surfacementioning

confidence: 99%

Lacritin and other autophagy associated proteins in ocular surface health

Karnati

Talla²,

Peterson³

et al. 2016

Experimental Eye Research

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Advantage may be taken of macroautophagy (‘autophagy’) to promote ocular health. Autophagy continually captures aged or damaged cellular material for lysosomal degradation and recyling. When autophagic flux is chronically elevated, or alternatively deficient, health suffers. Chronic elevation of flux and stress are the consequence of inflammatory cytokines or of dry eye tears but not normal tears in vitro. Exogenous tear protein lacritin transiently accelerates flux to restore homeostasis in vitro and corneal health in vivo, and yet the monomeric active form of lacritin appears to be selectively deficient in dry eye. Tissue transglutaminase-dependent cross-linking of monomer decreases monomer quantity and monomer affinity for coreceptor syndecan-1 thereby abrogating activity. Tissue transglutaminase is elevated in dry eye. Mutation of arylsulfatase A, arylsulfatase B, ceroid-lipofuscinosisneuronal 3, mucolipin, or Niemann-Pick disease type C1 respectively underlie several diseases of apparently insufficient autophagic flux that affect the eye, including: metachromatic leukodystrophy, mucopolysaccharidosis type VI, juvenile-onset Batten disease, mucolipidosis IV, and Niemann-Pick type C associated with myelin sheath destruction of corneal sensory and ciliary nerves and of the optic nerve; corneal clouding, ocular hypertension, glaucoma and optic nerve atrophy; accumulation of ‘ceroid-lipofuscin’ in surface conjunctival cells, and in ganglion and neuronal cells; decreased visual acuity and retinal dystrophy; and neurodegeneration. For some, enzyme or gene replacement, or substrate reduction, therapy is proving to be successful. Here we discuss examples of restoring ocular surface homeostasis through alteration of autophagy, with particular attention to lacritin.

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Expression of growth factors in the conjunctiva from patients with active trachoma

Cited by 18 publications

References 38 publications

Simultaneous Transcriptional Profiling of Bacteria and Their Host Cells

Simultaneous Transcriptional Profiling of Bacteria and Their Host Cells

Immunohistochemical Detection of CTGF in the Human Eye

Lacritin and other autophagy associated proteins in ocular surface health

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