Biomedical subjects

M A Pavilack

Publications and source records attributed to M A Pavilack.

8 recordsLinked to original sources

PubMed1992

Through curettage in the treatment of chronic canaliculitis.

While various techniques have been proposed for the treatment of canaliculitis, there have been no published series that evaluate the efficacy of simple curettage in the treatment of persistent or recurrent canaliculitis. We report the effectiveness of thorough, simple curettage (without canaliculotomy) in 11 patients with chronic canaliculitis. All patients had a history of canaliculitis-related symptoms for a minimum of 6 months and clinically detectable canalicular concretions before initial treatment. Thorough, simple curettage (without canaliculotomy) resolved the chronic canaliculitis in all of the patients. Ten of the 11 patients were cured with a maximum of two sessions of curettage. One patient required three treatments of curettage and silicone intubation for common canalicular narrowing to render her free of symptoms. No surgical complications occurred in any of the patients. Our report confirms the effectiveness and low morbidity of thorough curettage in the treatment of persistent or recurrent cases of canaliculitis.

Adult↗

PubMed1992

Intercellular adhesion molecule-1 (ICAM-1) and HLA-DR antigens in herpes keratitis.

PURPOSE: Intercellular adhesion molecule-1 (ICAM-1) is a cell surface glycoprotein that binds leukocyte function antigen-1 receptor on leukocytes, thereby regulating leukocyte trafficking and function at sites of inflammation. Recently, the authors demonstrated ICAM-1 in human corneas exposed to proinflammatory cytokines, but ICAM-1 has not been reported in corneal disease. In this study, the presence of ICAM-1 in human disciform herpes simplex virus (HSV) keratitis is investigated. METHODS: Immunohistochemistry was performed for ICAM-1 on 4 keratoplasty specimens from patients with corneal scarring due to disciform HSV keratitis and 1 corneoscleral biopsy of a patient with active HSV keratoscleritis using specific, characterized monoclonal antibody to ICAM-1. Negative immunohistochemical controls included monoclonal antibodies to other vascular endothelial adhesion molecules or mouse serum. RESULTS: All 5 specimens demonstrated intense ICAM-1 immunoreactivity of keratinocytes, stromal keratocytes, and endothelial cells, predominantly in regions of leukocytic infiltration. Diffuse, intense HLA-DR positivity was detected throughout the corneas. The specimens failed to react with control antibodies. CONCLUSION: These results are the first to demonstrate ICAM-1 in human corneal disease and suggest important roles for ICAM-1 and HLA-DR co-expression in generating immune responses in HSV keratitis. Increased ICAM-1 expression in regions of leukocytic infiltration may regulate leukocyte-corneal cell binding, thereby promoting immune responses and damage by activated leukocytes.

Adult↗

PubMed1992

Pneumotonometry using sterile single-use tonometer covers.

Current methods for cleaning pneumotonometer tips include soaking the removable tip in various chemical agents. Disadvantages of this technique include the potential for incomplete disinfection, corneal contact with cleaning solutions, tip damage or loss, and soaking time. The authors studied the use of an available, disposable latex cover placed over the pneumotonometer tip for measuring intraocular pressure (IOP) in 46 eyes with normal corneas from a glaucoma screening clinic and 141 eyes with normal and abnormal corneas from a cornea and external disease clinic. The mean absolute IOP difference comparing with and without the tonometer cover was 1.6 mmHg for the glaucoma screening patients and 1.8 mmHg for the cornea clinic patients. A tonographic-like effect due to repeated tonometry also was shown. An additional study measuring a series of known IOP values in a cadaver eye showed no significant difference between uncovered and covered readings. These data suggest that placement of a disposable, latex cover over the pneumotonometer tip enables accurate IOP measurements and is a sanitary and convenient alternative method to repeated chemical disinfection.

Adolescent↗

PubMed1992

Modulation and function of intercellular adhesion molecule-1 (CD54) on human retinal pigment epithelial cells.

As part of the blood-retina barrier, the neuroectodermally-derived retinal pigment epithelial (RPE) monolayer is strategically positioned to interact with circulating leukocytes and regulate their access to the retina. We, therefore, studied whether human RPE cells express intercellular adhesion molecule-1 (ICAM-1), a specialized cell surface glycoprotein that binds the leukocyte function antigen-1 receptor present on all leukocytes. Using specific monoclonal antibody to ICAM-1, immunohistochemical staining of freshly-isolated primary and fourth passaged human RPE cells resulted in delicate reaction product that increased dramatically upon exposure to human recombinant (r) interferon-gamma (rIFN-gamma), interleukin-1-beta (rIL-1 beta), or tumor necrosis factor-alpha (rTNF-alpha). Fluorescence-activated cell sorting analysis demonstrated 2-fold increases in constitutive RPE ICAM-1 expression within 6 hours of exposure to physiologic concentrations of rIFN-gamma, rIL-1 beta, or rTNF-alpha. In standardized leukocyte adherence assays, cultured RPE cells showed avid binding of neutrophils that increased significantly after stimulation with rIFN-gamma, rIL-1 beta, or rTNF-alpha (p less than 0.001). In parallel assays, monoclonal antibody to either ICAM-1 on RPE cells, or subunits of leukocyte function antigen-1 receptors on leukocytes significantly blocked leukocyte binding to unstimulated (p less than 0.001) or rIFN-gamma-stimulated RPE cells (p less than 0.001). To demonstrate RPE ICAM-1 expression in intact human tissue, fresh uveoretinal explants were exposed to rIFN-gamma, rIL-1 beta, or rTNF-alpha and stained using mAb to ICAM-1. Tissue sections of cytokine-stimulated explants revealed dramatic increases in RPE ICAM-1 immunoreactivity over the low levels observed in unstimulated uveoretinal tissue. Our results indicate that: (a) ICAM-1 is expressed at low levels on unstimulated RPE cells, (b) RPE ICAM-1 may be augmented by inflammatory cytokines, and (c) RPE ICAM-1 is a functional receptor mediating leukocyte binding. ICAM-1 on RPE cells at the blood-retina barrier may regulate leukocytic infiltration in ocular diseases in which leukocytes are important pathogenetically and may be important to the generation of ocular immune responses.

Cell Adhesion↗

PubMed1992

Differential expression of human corneal and perilimbal ICAM-1 by inflammatory cytokines.

The mechanisms that regulate corneal infiltration by circulating leukocytes in inflammatory diseases are poorly understood. In this study, we investigated the effects of pro-inflammatory cytokines on corneal endothelial (CE) and stromal (CS) expression of intercellular adhesion molecule-1 (ICAM-1), a specialized cell surface glycoprotein that binds the leukocyte function antigen-1 (LFA-1) receptor present on all leukocytes and enhances immune responses. Using specific monoclonal antibody (mAb) to ICAM-1, immunohistochemical staining of intact human corneas resulted in discrete, granular reaction product in CE and CS cells as well as perilimbal vascular endothelium that increased dramatically when exposed to human recombinant interleukin-1-beta (rIL-1 beta), tumor necrosis factor-alpha (rTNF-alpha), and interferon-gamma (rIFN-gamma). Immunoreactive ICAM-1 in CE and CS cells was differentially increased by each of these cytokines. In contrast, immunoreactive endothelial-leukocyte adhesion molecule-1 and vascular cell adhesion molecule-1 were not detected in any CE or CS cells of unstimulated or cytokine-stimulated corneas. In standardized leukocyte adherence assays, neutrophil binding to CE surfaces of whole corneas increased significantly upon exposure to rIL-1 beta, rTNF-alpha, or rIFN-gamma (P less than 0.001). In parallel assays, mAb to ICAM-1 on CE cells or subunits of LFA-1 receptors on leukocytes, but not control mAb, significantly blocked leukocyte binding to unstimulated (P less than 0.01) or rIFN-gamma-stimulated corneas (P less than 0.001). Our results indicate that: (1) ICAM-1 is expressed at low levels on unstimulated CE cells, CS cells, and perilimbal vascular endothelium; (2) ICAM-1 may be augmented differentially in corneal and perilimbal tissue by pro-inflammatory cytokines; and (3) ICAM-1 is a functional ligand mediating corneal-leukocyte binding. Differential expression of ICAM-1 within corneal tissue may regulate keratitic precipitate formation, leukocyte trafficking and accumulation, and localized generation of immune responses.

Cell Adhesion Molecules↗

PubMed1991

Human and monkey corneal endothelium expression of low-density lipoprotein receptors.

Receptors for low-density lipoprotein are necessary for high-affinity uptake of lipid and protein essential to cell structure and function. Distinct receptors for acetoacetylated low-density lipoprotein internalize oxidized or enzymatically modified low-density lipoprotein and extracellular matrix components. We identified low-density lipoprotein receptors on cultured human and monkey corneal endothelial cells by the avid incorporation of fluorescently labeled low-density lipoprotein that was competitively inhibited by excess unlabeled low-density lipoprotein but not by unlabeled acetoacetylated low-density lipoprotein. Specific uptake of labeled low-density lipoprotein was greatest in nonconfluent, growing cells and increased after low-density lipoprotein deprivation. Intact endothelial monolayers of whole human cornea also incorporated low-density lipoprotein but not acetoacetylated low-density lipoprotein. After scratch injury of human corneas, spreading endothelium adjacent to areas of cell loss internalized more fluorescent low-density lipoprotein than cells distant from the injury. Blood-aqueous barrier breakdown occurring in ocular diseases and after surgical and nonsurgical trauma may allow leakage of circulating low-density lipoprotein, which provides a rich supply of lipid and protein for endothelial use. Efficient, receptor-mediated, low-density lipoprotein uptake may facilitate repair of damaged corneal endothelial membranes and regeneration of intact, functional cell monolayers.

Acetoacetates↗

PubMed1991

Intercellular adhesion molecule-1 in human corneal endothelium. Modulation and function.

The endothelium lining the posterior corneal surface performs physiologic pump functions essential to corneal clarity and integrity. A hallmark of keratitis, anterior ocular inflammation, and corneal allograft rejection is leukocyte adherence to the corneal endothelium (CE) forming keratitic precipitates. To elucidate mechanisms governing cornea-leukocyte interactions, cultured human CE cells and intact corneas were examined for expression of intercellular adhesion molecule-1 (ICAM-1), which binds the lymphocyte function-associated antigen-1 (LFA-1) on all leukocytes and enhances delayed-type hypersensitivity mediated by class II major histocompatibility complex antigens. Immunohistochemistry on culture CE cells using monoclonal anti-ICAM-1 antibody yield positive staining that increased after exposure to interleukin-1-beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (gamma-IFN). Standard leukocyte adherence assays demonstrated ICAM-1-mediated CE-neutrophil binding, which was specifically blocked by antibody to ICAM-1 or antibodies to LFA-1 on neutrophils. In whole human corneas, gamma-IFN increased CE and stromal keratocyte ICAM-1 immunoreactivity and enhanced CE-neutrophil adherence. As in CE cell cultures, antibody to ICAM-1 effectively blocked neutrophil binding to the CE cells of whole corneas. These results are the first to demonstrate ICAM-1 in ocular tissue. They indicate that CE cells express functional ICAM-1, which may be modulated by inflammatory cytokines, ICAM-1 provides mechanisms for keratitic precipitate formation, regulation of corneal leukocyte trafficking and the generation of immune responses that may be crucial to allograft rejection.

Cell Adhesion Molecules↗

PubMed1991

Human corneal interleukin-8. IL-1 and TNF-induced gene expression and secretion.

Corneal leukocytic infiltration is an important component of numerous ocular diseases, but specific corneal-derived leukocyte chemotaxins have not been identified. In this study, the authors identified interleukin-8 (IL-8), a known neutrophil and lymphocyte chemotaxin, to be an important chemotaxin produced by human corneal tissue. In situ hybridization and immunohistochemistry of corneas exposed to human recombinant (r) interleukin-1-beta (rIL-1 beta) or tumor necrosis factor-alpha (rTNF-alpha) revealed significant increases in corneal endothelial and stromal cell IL-8 mRNA (P less than 0.001) and marked increases in cell-associated immunoreactive IL-8 compared with unstimulated controls. ELISA assays revealed four- to eight-fold increases in corneal IL-8 secretion after 24-hour exposures to either cytokine over that obtained with unstimulated corneas (P = 0.01). In neutrophil chemotactic bioassays, significant increases in functional IL-8 were detected in media conditioned by corneas exposed to rIL-1 beta or rTNF-alpha for 24 hours (P less than 0.001). Preincubation of these corneal media with anti-IL-8 antibody significantly reduced neutrophil chemotaxis by more than 80%. These results suggest that the cornea is an active participant in ocular inflammation and raise the possibility that agents used in experimental corneal pocket models may produce indirect effects by inducing corneal secretion of other factors, such as IL-8.

Chemotaxis, Leukocyte↗