Is Autologous Serum a Tonic for the Ailing Corneal Epithelium?

Pflugfelder, Stephen C.

doi:10.1016/j.ajo.2006.05.002

Cited by 32 publications

(25 citation statements)

References 13 publications

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“…Unfortunately, conventional therapies, such as artificial tears and bandage contact lenses, often fail. 27 The present study demonstrates that topical insulin to accelerate corneal reepithelialization has many advantages to offer, including cost-effectiveness, increased patient compliance, ease of delivery, independence of systemic serum glucose levels, specificity for diabetic keratopathy, avoidance of first-pass metabolism, fast rate of absorption and effectiveness, minimal immunological reactions, and no tolerance or adverse effects. Moreover, insulin administered long-term to the human eye at concentrations of up to 100 U/mL for 8 weeks in isotonic sodium chloride solution has been shown not to be toxic.…”

Section: Commentmentioning

confidence: 99%

Use of Topical Insulin to Normalize Corneal Epithelial Healing in Diabetes Mellitus

Zagon

Klocek

Sassani³

et al. 2007

Arch Ophthalmol

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Section: Commentmentioning

confidence: 99%

Use of Topical Insulin to Normalize Corneal Epithelial Healing in Diabetes Mellitus

Zagon

Klocek

Sassani³

et al. 2007

Arch Ophthalmol

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“…1 Diabetic corneal complications, termed diabetic keratopathy, are resistant to conventional treatment regimens. 2,3 Patients with diabetic keratopathy usually do not have detectable symptoms; however, once the cornea is injured, delayed epithelium-wound healing is often observed. 4 Delayed epithelial wound closure may be associated with sight-threatening complications, such as stromal opacification, surface irregularity, and microbial keratitis.…”

mentioning

confidence: 99%

“…4 Delayed epithelial wound closure may be associated with sight-threatening complications, such as stromal opacification, surface irregularity, and microbial keratitis. 2 Like diabetic skin wounds, there is an unmet need for effective treatments of persistent wounds and ulceration in the DM cornea. Hence, a better understanding of the mechanisms underlying pathophysiology of delayed epithelium-wound healing in DM tissues is needed.…”

mentioning

confidence: 99%

Targeting Imbalance between IL-1β and IL-1 Receptor Antagonist Ameliorates Delayed Epithelium Wound Healing in Diabetic Mouse Corneas

Yan

Gao

Sun

et al. 2016

The American Journal of Pathology

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fanxq@sh163. net.Patients with diabetes mellitus often develop corneal complications and delayed wound healing. How diabetes might alter acute inflammatory responses to tissue injury, leading to delayed wound healing, remains mostly elusive. Using a streptozotocin-induced type I diabetes mellitus mice and corneal epithelium-debridement wound model, we discovered that although wounding induced marked expression of IL-1b and the secreted form of IL-1 receptor antagonist (sIL-1Ra), diabetes suppressed the expressions of sIL-1Ra but not IL-1b in healing epithelia and both in whole cornea. In normoglycemic mice, IL-1b or sIL-1Ra blockade delayed wound healing and influenced each other's expression. In diabetic mice, in addition to delayed reepithelization, diabetes weakened phosphatidylinositol 3-kinaseeAkt signaling, caused cell apoptosis, diminished cell proliferation, suppressed neutrophil and natural killer cell infiltrations, and impaired sensory nerve reinnervation in healing mouse corneas. Local administration of recombinant IL-1Ra partially, but significantly, reversed these pathological changes in the diabetic corneas. CXCL10 was a downstream chemokine of IL-1beIL-1Ra, and exogenous CXCL10 alleviated delayed wound healing in the diabetic, but attenuated it in the normal corneas. In conclusion, the suppressed early innate/inflammatory responses instigated by the imbalance between IL-1b and IL-1Ra is an underlying cause for delayed wound healing in the diabetic corneas. Local application of IL-1Ra accelerates reepithelialization and may be used to treat chronic corneal and potential skin wounds of diabetic patients. (Am J Pathol 2016 http://dx

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“…19 -21 Prolonged corneal epithelial defects due to a delay in wound healing may result in sight-threatening complications, including corneal opacity, neovascularization, and microbial keratitis. 22,23 In the wounded cornea, the epithelium plays a central role, as a key cell type in repairing the cornea and as the source of several growth factors. 19,20 In addition to the epithelial cells, innate immune cells, such as polymorphonuclear leukocytes (PMNs) and ␥␦T cells, have also been involved in the regulation of epithelial wound healing in vivo.…”

mentioning

confidence: 99%

Dendritic Cell–Epithelium Interplay Is a Determinant Factor for Corneal Epithelial Wound Repair

Gao

Yin

Yoon

et al. 2011

The American Journal of Pathology

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The functions of intraepithelial dendritic cells (DCs) are critical for mucosal innate and adaptive immunity, but little is known about the role of tissue-specific DCs in epithelial homeostasis and tissue repair. By using the epithelial debridement wound model and CD11c-diphtheria toxin receptor mice that express a CD11c promoter-driven diphtheria toxin receptor, we showed that DCs migrate along with the epithelial sheet to cover the wound and that local depletion of DCs resulted in a significant delay in epithelial wound closure. In response to wounding, migratory epithelia produce CXCL10, thymic stromal lymphopoietin, and IL-1␤ and its antagonist soluble IL-1 receptor antagonist (sIL-1Ra); depletion of corneal DCs reversed their elevated expressions to a different extent, suggesting a DC-mediated positive feedback loop in epithelial gene expression. Furthermore, both CXCL10 and thymic stromal lymphopoietin were localized in migratory epithelia, suggesting that epithelial cells play a key role in DC infiltration and activation in injured corneas. On the other hand, DC depletion resulted in suppressed epithelial AKT activation, increased cell apoptosis, and decreased polymorphonuclear leukocyte infiltration in the healing cornea. These results indicate that DCs and epithelium form a functional entity at mucosal surfaces for maintaining corneal homeostasis and for tissue repair.

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Is Autologous Serum a Tonic for the Ailing Corneal Epithelium?

Cited by 32 publications

References 13 publications

Use of Topical Insulin to Normalize Corneal Epithelial Healing in Diabetes Mellitus

Use of Topical Insulin to Normalize Corneal Epithelial Healing in Diabetes Mellitus

Targeting Imbalance between IL-1β and IL-1 Receptor Antagonist Ameliorates Delayed Epithelium Wound Healing in Diabetic Mouse Corneas

Dendritic Cell–Epithelium Interplay Is a Determinant Factor for Corneal Epithelial Wound Repair

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