Lecithin-bound superoxide dismutase in the prevention of neutrophil- induced damage of corneal tissue

Koki Matsumoto, Shigeto Shimmura, Eiki Goto, Keiko Saito, Tsutomu Takeuchi, Seiya Miyajima, Akira Negi, Kazuo Tsubota

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

PURPOSE. To evaluate the effects of a lipophilic analog of superoxide dismutase (SOD) in the prevention of polymorphonuclear leukocyte (PMN)- induced damage to corneal epithelial cells in vitro and in bacterial corneal ulcers in vivo. METHODS. Immortalized human corneal epithelial cells (T- HCEC) were cocultured with human PMNs activated with N-formyl-methionyl- leucyl-phenylalanine for 18 hours, after which lactate dehydrogenase (LDH) activity of the supernatant was measured as a marker of cellular damage. The inhibitory effects of lecithin-bound SOD (PC-SOD) and unmodified SOD, as well as PMNs pretreated with anti-CD 18 monoclonal antibody, were compared with untreated control. The retention of each drug on the ocular surface of healthy volunteers was measured by flow cytometry using brush cytology samples. The protective effects of a 0.1% solution of PC-SOD on Pseudomonas aeruginosa corneal infection in guinea pigs were assessed by inflammatory grading scores and histology. RESULTS. Both PC-SOD and SOD effectively suppressed PMN-induced LDH release in T-HCEC in a dose-dependent manner. LDH release was also attenuated when PMNs were pretreated with anti-CD 18 antibodies, suggesting that adhesion molecules were involved in the process. Brush cytology of conjunctival samples showed that PC-SOD was retained longer on the ocular surface compared with unmodified SOD. PC-SOD significantly prevented excessive tissue damage by infiltrating PMNs in P. aeruginosa corneal infection, whereas in control eyes, perforation of the cornea occurred by 6 days. CONCLUSIONS. PC-SOD was effective in attenuating PMN- related tissue damage to corneal tissue both in vitro and in P. aeruginosa infection in guinea pigs.

Original languageEnglish
Pages (from-to)30-35
Number of pages6
JournalInvestigative Ophthalmology and Visual Science
Volume39
Issue number1
Publication statusPublished - 1998 Jan
Externally publishedYes

Fingerprint

Lecithins
Superoxide Dismutase
Neutrophils
L-Lactate Dehydrogenase
Pseudomonas aeruginosa
Cell Biology
Guinea Pigs
Corneal Injuries
Epithelial Cells
N-Formylmethionine Leucyl-Phenylalanine
Corneal Ulcer
Pseudomonas Infections
Infection
Cornea
Histology
Healthy Volunteers
Flow Cytometry
Monoclonal Antibodies

ASJC Scopus subject areas

  • Ophthalmology

Cite this

Lecithin-bound superoxide dismutase in the prevention of neutrophil- induced damage of corneal tissue. / Matsumoto, Koki; Shimmura, Shigeto; Goto, Eiki; Saito, Keiko; Takeuchi, Tsutomu; Miyajima, Seiya; Negi, Akira; Tsubota, Kazuo.

In: Investigative Ophthalmology and Visual Science, Vol. 39, No. 1, 01.1998, p. 30-35.

Research output: Contribution to journalArticle

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abstract = "PURPOSE. To evaluate the effects of a lipophilic analog of superoxide dismutase (SOD) in the prevention of polymorphonuclear leukocyte (PMN)- induced damage to corneal epithelial cells in vitro and in bacterial corneal ulcers in vivo. METHODS. Immortalized human corneal epithelial cells (T- HCEC) were cocultured with human PMNs activated with N-formyl-methionyl- leucyl-phenylalanine for 18 hours, after which lactate dehydrogenase (LDH) activity of the supernatant was measured as a marker of cellular damage. The inhibitory effects of lecithin-bound SOD (PC-SOD) and unmodified SOD, as well as PMNs pretreated with anti-CD 18 monoclonal antibody, were compared with untreated control. The retention of each drug on the ocular surface of healthy volunteers was measured by flow cytometry using brush cytology samples. The protective effects of a 0.1{\%} solution of PC-SOD on Pseudomonas aeruginosa corneal infection in guinea pigs were assessed by inflammatory grading scores and histology. RESULTS. Both PC-SOD and SOD effectively suppressed PMN-induced LDH release in T-HCEC in a dose-dependent manner. LDH release was also attenuated when PMNs were pretreated with anti-CD 18 antibodies, suggesting that adhesion molecules were involved in the process. Brush cytology of conjunctival samples showed that PC-SOD was retained longer on the ocular surface compared with unmodified SOD. PC-SOD significantly prevented excessive tissue damage by infiltrating PMNs in P. aeruginosa corneal infection, whereas in control eyes, perforation of the cornea occurred by 6 days. CONCLUSIONS. PC-SOD was effective in attenuating PMN- related tissue damage to corneal tissue both in vitro and in P. aeruginosa infection in guinea pigs.",
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N2 - PURPOSE. To evaluate the effects of a lipophilic analog of superoxide dismutase (SOD) in the prevention of polymorphonuclear leukocyte (PMN)- induced damage to corneal epithelial cells in vitro and in bacterial corneal ulcers in vivo. METHODS. Immortalized human corneal epithelial cells (T- HCEC) were cocultured with human PMNs activated with N-formyl-methionyl- leucyl-phenylalanine for 18 hours, after which lactate dehydrogenase (LDH) activity of the supernatant was measured as a marker of cellular damage. The inhibitory effects of lecithin-bound SOD (PC-SOD) and unmodified SOD, as well as PMNs pretreated with anti-CD 18 monoclonal antibody, were compared with untreated control. The retention of each drug on the ocular surface of healthy volunteers was measured by flow cytometry using brush cytology samples. The protective effects of a 0.1% solution of PC-SOD on Pseudomonas aeruginosa corneal infection in guinea pigs were assessed by inflammatory grading scores and histology. RESULTS. Both PC-SOD and SOD effectively suppressed PMN-induced LDH release in T-HCEC in a dose-dependent manner. LDH release was also attenuated when PMNs were pretreated with anti-CD 18 antibodies, suggesting that adhesion molecules were involved in the process. Brush cytology of conjunctival samples showed that PC-SOD was retained longer on the ocular surface compared with unmodified SOD. PC-SOD significantly prevented excessive tissue damage by infiltrating PMNs in P. aeruginosa corneal infection, whereas in control eyes, perforation of the cornea occurred by 6 days. CONCLUSIONS. PC-SOD was effective in attenuating PMN- related tissue damage to corneal tissue both in vitro and in P. aeruginosa infection in guinea pigs.

AB - PURPOSE. To evaluate the effects of a lipophilic analog of superoxide dismutase (SOD) in the prevention of polymorphonuclear leukocyte (PMN)- induced damage to corneal epithelial cells in vitro and in bacterial corneal ulcers in vivo. METHODS. Immortalized human corneal epithelial cells (T- HCEC) were cocultured with human PMNs activated with N-formyl-methionyl- leucyl-phenylalanine for 18 hours, after which lactate dehydrogenase (LDH) activity of the supernatant was measured as a marker of cellular damage. The inhibitory effects of lecithin-bound SOD (PC-SOD) and unmodified SOD, as well as PMNs pretreated with anti-CD 18 monoclonal antibody, were compared with untreated control. The retention of each drug on the ocular surface of healthy volunteers was measured by flow cytometry using brush cytology samples. The protective effects of a 0.1% solution of PC-SOD on Pseudomonas aeruginosa corneal infection in guinea pigs were assessed by inflammatory grading scores and histology. RESULTS. Both PC-SOD and SOD effectively suppressed PMN-induced LDH release in T-HCEC in a dose-dependent manner. LDH release was also attenuated when PMNs were pretreated with anti-CD 18 antibodies, suggesting that adhesion molecules were involved in the process. Brush cytology of conjunctival samples showed that PC-SOD was retained longer on the ocular surface compared with unmodified SOD. PC-SOD significantly prevented excessive tissue damage by infiltrating PMNs in P. aeruginosa corneal infection, whereas in control eyes, perforation of the cornea occurred by 6 days. CONCLUSIONS. PC-SOD was effective in attenuating PMN- related tissue damage to corneal tissue both in vitro and in P. aeruginosa infection in guinea pigs.

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