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H L Sumner

Publications and source records attributed to H L Sumner.

11 recordsLinked to original sources
PubMed1998

Cytokine expression in a rat model of Staphylococcus aureus endophthalmitis.

PURPOSE: To examine the ability of viable Staphylococcus aureus to induce the production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, cytokine-induced neutrophil chemoattractant (CINC), and interferon (IFN)-gamma after intravitreal injection. METHODS: Experimental rat eyes were injected with a 25-microl volume of approximately 80 colony-forming units of viable S. aureus; control eyes received sterile saline. Eyes were graded daily for signs of clinical inflammation and were removed 6, 24, 48, and 72 hours after injection. One group was prepared for histologic analysis, and vitreous was removed from the other group for cytokine analysis, using standard enzyme-linked immunosorbent assay procedures. RESULTS: TNF-alpha, IL-1beta, CINC, and IFN-gamma were detected in experimental vitreous samples at increased levels that peaked at 24 hours. TNF-alpha, IL-1beta, and CINC declined at 48 hours, but IFN-gamma remained elevated. At 72 hours, levels returned to baseline. Statistically significant elevations of TNF-alpha, IL-1beta, and CINC were detected in experimental samples at 24, but not at 6 and 48 hours compared with levels in saline control samples (P < 0.03). A statistically significant increase in IFN-gamma was detected at 24 and 48 hours compared with control levels (P < 0.03). In experimental animals, clinical inflammation and inflammatory cells peaked at 24 hours, persisted at 48 hours, and began to decline thereafter. Neutrophils were the predominant inflammatory cell detected at 24 (72.3% of cells) and 48 (60.1%) hours. By 72 hours, the total number of inflammatory cells had decreased by 75.0%, and the cellular infiltrate had changed so that neutrophils equaled monocytes-macrophages. CONCLUSIONS: S. aureus induced the expression of TNF-alpha, IL-1beta, CINC, and IFN-gamma. The time course of these cytokine levels could account for the clinical inflammatory responses and the entry and decline of vitreous cells in this model of bacterial endophthalmitis.

Animals↗
PubMed1996

Generation of complement membrane attack complex in normal human corneas.

PURPOSE: To determine whether complement-derived SC5b-9, the soluble nonlytic-fluid phase of the membrane attack complex, can be generated in normal human corneas when they are injured with lipopolysaccharide (LPS), ribitol teichoic acid (RTA) immune complexes, acid, or alkali. METHODS: The experimental cornea of each donor pair was injected with 50 microliters of sterile saline containing 0.5 mg of LPS or 50 microliters of sterile saline containing 250 micrograms of RTA immune complexes. Other experimental corneas were treated topically for 35 seconds with either 200 microliters of 1N HCl or 2N NaOH. The control cornea of each donor pair was injected with 50 microliters of sterile saline or was treated topically for 35 seconds with 200 microliters of sterile saline. After injury, all corneas were incubated in medium 199 for 6 hours at 37 degrees C in 5% CO2, then eluted for 24 hours in phosphate-buffered saline with 10 mM ethylenediaminetetraacetic acid. Each corneal eluate was collected and stored at -70 degrees C until assayed for SC5b-9 by an enzyme immunoassay. RESULTS: Compared with control corneas, SC5b-9 levels were increased significantly in corneas injected with LPS or RTA immune complexes. However, when compared with controls, SC5b-9 levels were decreased significantly in corneas treated with HCl or NaOH. CONCLUSIONS: Normal human corneas injured immunologically with LPS or RTA immune complexes activate the classical or alternate pathway and generate SC5b-9. Corneas injured chemically with acid or alkali do not produce SC5b-9.

Adult↗
PubMed1994

Complement system and host defense against staphylococcal endophthalmitis.

PURPOSE: The authors studied the role of the complement system in host defense against Staphylococcus epidermidis and S. aureus endophthalmitis. METHODS: Guinea pigs in the S. epidermidis model received an intravitreal injection of 7000 viable organisms, and guinea pigs in the S. aureus model received 50 viable organisms. The experimental animals in each model were decomplemented with intraperitoneal (IP) injections of cobra venom factor, whereas the control animals received IP injections of normal saline. Mean log bacterial counts in the vitreous and mean serum complement titers were compared in the experimental and control animals in each model on days 1, 2, 3, and 7. RESULTS: In the S. epidermidis model, mean log bacterial counts in the vitreous were significantly higher in the experimental group than the control group on days 1 and 2 (P < 0.01) and on day 3 (P < 0.05). Mean serum complement titers were significantly lower in the experimental group at all days (P < 0.01). In the S. aureus model, mean log bacterial counts in the vitreous were significantly higher in the experimental group than the control group on day 2 (P < 0.05) and day 3 (P < 0.01). Mean serum complement titers were significantly lower in the experimental group on days 1, 2, and 3 (P < 0.01), but not on day 7. CONCLUSION: These results suggest that decomplemented guinea pigs show impaired host defense to S. epidermidis and S. aureus endophthalmitis and that this defense is restored as complement levels approach normal.

Animals↗
PubMed1992

The effect of systemic decomplementation with cobra venom factor on corneal complement levels in guinea pigs.

The authors examined the effect of systemic administration of cobra venom factor (CVF) on hemolytic complement levels in guinea pig sera and corneas. Guinea pigs received repeated intraperitoneal injections of CVF. Sera and corneas were obtained before and 1, 2, 5, 8, 10, 12, 16, and 20 d after the initial injection of CVF. Total hemolytic complement activity was measured by lysis of sheep erythrocytes sensitized with rabbit antibodies. There was a significant decrease in serum complement levels at days 1, 2, 5, 8, and 10 after the initial injection of CVF. After this, complement levels rose to levels that exceeded preinjection values. Complement levels in corneas also declined after CVF injections with a significant decrease at days 2, 5, 8, and 10 and a return to normal thereafter. Corneal complement depletion and restoration lagged behind serum. Moreover, the rate of complement depletion and restoration was greater for serum than cornea. Light microscopic examination of representative corneas at each time did not show local tissue changes during decomplementation. This is first study (to the authors' knowledge) to document corneal complement depletion by systemic administration of CVF. Low-to-absent corneal complement levels were present 2 d after the initial injection of CVF and persisted for 6 d. This model could be used to study the influence of complement on traumatic and immunologic injuries to the cornea.

Animals↗
PubMed1990

Inflammatory mediators in the vitreous humor of AIDS patients with retinitis.

We measured levels of protein, of complement-derived anaphylatoxins (C3a, C4a, and C5a), and of the lymphokines interleukin-2 and gamma interferon, in vitreous humor from 10 AIDS patients with vitritis and retinitis (group 1). We compared these measurements with levels in vitreous from 7 patients with vitritis but without AIDS (group 2), 10 patients with vitreous hemorrhages (group 3), and 20 patients with retinal detachments or epiretinal membranes without clinical evidence of vitreal inflammation (group 4). Vitreous humor from 10 AIDS patients had measurable levels of interleukin-2 in three of nine samples, gamma interferon in six of nine samples, C3a and C4a in all ten samples, and C5a in only one of ten samples. Vitreous humor from group 1 did not differ significantly from vitreous from group 2. On the other hand, vitreous from group 1 had significantly higher levels of gamma interferon, C3a, and C4a, and higher ratios of these anaphylatoxins to protein, in comparison to vitreous in groups 3 and 4. The results of this study suggest that vitreous humor from AIDS patients with retinitis contains activated complement and may contain interleukin-2 and gamma interferon. Viral retinitis is associated with the presence of lymphokines in vitreous humor. Additionally, anaphylatoxin and gamma interferon levels, but not interleukin-2 levels, correlate with vitreal inflammation. This is the first study to measure interleukin-2, gamma interferon, and C5a levels in human vitreous humor.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Generation of complement-derived anaphylatoxins in normal human donor corneas.

Complement-derived anaphylatoxins (C3a, C4a, and C5a) are potent, stable mediators of acute inflammation. Because human corneas contain functional complement, the authors subjected normal human donor corneas to various forms of immunologic or chemical injury to determine if the complement system could be activated and anaphylatoxins generated. The experimental cornea of each donor pair was injected with lipopolysaccharide (LPS) or immune complexes or injured by application of acid or alkali. The remaining cornea of each donor pair served as a control. After incubation of corneas in tissue culture media for 6 hours and elution in phosphate-buffered saline for 24 hours, C3a, C4a, and C5a were measured in corneal eluates by radioimmunoassay. Compared with control corneas, C3a levels were significantly increased in corneas injected with LPS or immune complexes and in corneas injured with acid or alkali. C4a levels were significantly elevated in corneas injected with immune complexes and in corneas injured with acid or alkali but not in corneas injected with LPS. C5a levels were detectable only in corneas injured with acid or alkali. These results suggest that immunologic reactions in the human cornea may activate the classic or alternative complement pathways and generate anaphylatoxins. Additionally, chemical injuries with acid or alkali generate anaphylatoxins in the cornea. Anaphylatoxins may participate in the acute inflammatory response of the human cornea to chemical or immunologic injury.

Acids↗
PubMed1985

The complement system and host defense against Pseudomonas endophthalmitis.

The authors examined the role of the complement system in host defense against Pseudomonas aeruginosa endophthalmitis. Guinea pigs received intravitreal injections of P. aeruginosa, and comparisons were made between bacterial counts from the vitreous of control guinea pigs and experimental guinea pigs that underwent systemic decomplementation with cobra venom factor. In group 1 (intravitreal injection of 42 organisms), bacterial counts were significantly higher in the vitreous of decomplemented guinea pigs versus control guinea pigs at days 1, 2, and 3 after intravitreal injection but not at day 7 when complement levels returned to normal. In group 2 (intravitreal injection of 102 organisms), bacterial counts were significantly higher in the vitreous of experimental guinea pigs versus control guinea pigs only at day 1 with no statistically significant differences thereafter. In group 3 (intravitreal injection of 150 bacteria), there were no significant differences in bacterial counts in the vitreous of experimental versus control guinea pigs. Our results in group 1 suggest that partially decomplemented guinea pigs show impaired host defense to P. aeruginosa and that this defense is restored as complement levels return to normal. Intravitreal injection of higher numbers of P. aeruginosa as in a group 3 overwhelms and obscures any beneficial effect of the complement system on host defense.

Animals↗
PubMed1983

Experimental retinal autoimmunity (ERA) in strain 13 guinea pigs: induction of ERA-retinopathy with rhodopsin.

Strain 13 guinea pigs injected with either homologous or bovine rhodopsin, the visual pigment of the retinal outer segments, in complete Freund's adjuvant (CFA) developed experimental retinal autoimmunity (ERA). Initial clinical signs of disease were seen within 21 days after immunization. Pathologic examination of the eyes revealed the presence of inflammatory cells in the choroid and the destruction of the retinal rod outer segments. The unique feature of this disease is that despite the destruction of the inner and outer segments of the retina, at no time is there a substantial inflammatory cell infiltrate. Even as late as 45 days after immunization, when destruction of the retinal ganglion cell layer was noted, no inflammatory cells were detected in the retina. These findings suggest that the retinal inner and outer segments are the target of the autoimmune reaction subsequent to sensitization with purified rhodopsin-CFA.

Animals↗
PubMedDate not supplied

Complement-derived anaphylatoxins in human donor corneas treated with excimer laser.

BACKGROUND AND OBJECTIVE: An inflammatory response produced by excimer laser photorefractive keratectomy (PRK) may be associated with the subsequent corneal haze and regressions in refractive error observed after treatment. Complement-derived anaphylatoxins, potent mediators of inflammation, may have a role in postoperative healing. MATERIALS AND METHODS: Twenty right human donor corneas underwent a 6-D excimer laser PRK treatment. The corresponding left donor corneas served as the controls. After incubation in tissue culture media for 6 hours and elution in phosphate-buffered saline with EDTA for 24 hours, complement-derived anaphylatoxins C3a, C4a, and C5a were measured in corneal eluates by radioimmunoassay. RESULTS: Compared with control corneas, the excimer PRK corneas failed to demonstrate a significant increase in C3a, C4a, or C5a levels (P > .05). CONCLUSIONS: These results suggest that the excimer laser at this dose does not activate significant complement in the cornea.

Adolescent↗