Interleukin-10 knockout mice show increased inflammation in endotoxin-induced uveitis model

M. J. Balish, Stephen Planck, E. Balish, James (Jim) Rosenbaum, S. Hopkins

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Abstract

Purpose: Interleukin-10 (IL-10) has been shown to inhibit inflammation seen with endotoxin-induced uveitis in mice and rabbits. We studied mice genetically deficient in IL10 to see if they have increased inflammation in response to intravitreal endotoxin. Methods: Germ free (GF) and conventional (nGF) C57BL/6 X 129 mice genetically deficient for the IL-10 gene (IL-10KO) and congenic littermates showing IL-10 expression (IL-10+) underwent intravitreal injection of 1 /d (trial 1) or 2 1 (trial 2) of 125ng//tl endotoxin in buffer. At 24 hours the mice were euthanized. Inflammation was graded by a masked observer who counted leukocytes in a cross-section of the eye. Result: In trial 1, eleven GF IL-10KO mice had a mean ±SE of 72+25 cells per section (cps). Twelve nGFIL-10KOmicehadameanof70±46cps. Ten nGF IL-10+ mice had a mean of 13+9 cps. The difference in inflammation seen between IL-10+ and IL-10KO mice was statistically significant (p=0.02). In trial 2, eleven GF IL-10KO mice had a mean of 761 ±147 cps. Seven nGF IL-10KO mice had a mean of 1365±360 cps. Five GF IL10+ mice had a mean of 384±81 cps. Two nGF IL-10+ mice had a mean of 731 ±9 cps. This trend for more inflammation in the IL-10KO group did not reach statistical significance (p=0.11). Conclusion: Interleukin-10 knockout mice tend to develop more severe inflammation with endotoxin-induced uveitis at 24 hours than IL-10 competent mice. This lends support to the role of IL-10 as an anti-inflammatory cytokine. Although the germ free state should prevent exposure or tolerance to endotoxin, germ free mice in this study did not show a statistically significant increase in inflammation.

Original languageEnglish (US)
JournalInvestigative Ophthalmology and Visual Science
Volume38
Issue number4
StatePublished - 1997

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Uveitis
Knockout Mice
Endotoxins
Interleukin-10
Inflammation
129 Strain Mouse
Esotropia
Intravitreal Injections
Buffers
Leukocytes
Anti-Inflammatory Agents
Cytokines
Rabbits

ASJC Scopus subject areas

  • Ophthalmology

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Interleukin-10 knockout mice show increased inflammation in endotoxin-induced uveitis model. / Balish, M. J.; Planck, Stephen; Balish, E.; Rosenbaum, James (Jim); Hopkins, S.

In: Investigative Ophthalmology and Visual Science, Vol. 38, No. 4, 1997.

Research output: Contribution to journalArticle

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title = "Interleukin-10 knockout mice show increased inflammation in endotoxin-induced uveitis model",
abstract = "Purpose: Interleukin-10 (IL-10) has been shown to inhibit inflammation seen with endotoxin-induced uveitis in mice and rabbits. We studied mice genetically deficient in IL10 to see if they have increased inflammation in response to intravitreal endotoxin. Methods: Germ free (GF) and conventional (nGF) C57BL/6 X 129 mice genetically deficient for the IL-10 gene (IL-10KO) and congenic littermates showing IL-10 expression (IL-10+) underwent intravitreal injection of 1 /d (trial 1) or 2 1 (trial 2) of 125ng//tl endotoxin in buffer. At 24 hours the mice were euthanized. Inflammation was graded by a masked observer who counted leukocytes in a cross-section of the eye. Result: In trial 1, eleven GF IL-10KO mice had a mean ±SE of 72+25 cells per section (cps). Twelve nGFIL-10KOmicehadameanof70±46cps. Ten nGF IL-10+ mice had a mean of 13+9 cps. The difference in inflammation seen between IL-10+ and IL-10KO mice was statistically significant (p=0.02). In trial 2, eleven GF IL-10KO mice had a mean of 761 ±147 cps. Seven nGF IL-10KO mice had a mean of 1365±360 cps. Five GF IL10+ mice had a mean of 384±81 cps. Two nGF IL-10+ mice had a mean of 731 ±9 cps. This trend for more inflammation in the IL-10KO group did not reach statistical significance (p=0.11). Conclusion: Interleukin-10 knockout mice tend to develop more severe inflammation with endotoxin-induced uveitis at 24 hours than IL-10 competent mice. This lends support to the role of IL-10 as an anti-inflammatory cytokine. Although the germ free state should prevent exposure or tolerance to endotoxin, germ free mice in this study did not show a statistically significant increase in inflammation.",
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AU - Balish, M. J.

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AU - Hopkins, S.

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N2 - Purpose: Interleukin-10 (IL-10) has been shown to inhibit inflammation seen with endotoxin-induced uveitis in mice and rabbits. We studied mice genetically deficient in IL10 to see if they have increased inflammation in response to intravitreal endotoxin. Methods: Germ free (GF) and conventional (nGF) C57BL/6 X 129 mice genetically deficient for the IL-10 gene (IL-10KO) and congenic littermates showing IL-10 expression (IL-10+) underwent intravitreal injection of 1 /d (trial 1) or 2 1 (trial 2) of 125ng//tl endotoxin in buffer. At 24 hours the mice were euthanized. Inflammation was graded by a masked observer who counted leukocytes in a cross-section of the eye. Result: In trial 1, eleven GF IL-10KO mice had a mean ±SE of 72+25 cells per section (cps). Twelve nGFIL-10KOmicehadameanof70±46cps. Ten nGF IL-10+ mice had a mean of 13+9 cps. The difference in inflammation seen between IL-10+ and IL-10KO mice was statistically significant (p=0.02). In trial 2, eleven GF IL-10KO mice had a mean of 761 ±147 cps. Seven nGF IL-10KO mice had a mean of 1365±360 cps. Five GF IL10+ mice had a mean of 384±81 cps. Two nGF IL-10+ mice had a mean of 731 ±9 cps. This trend for more inflammation in the IL-10KO group did not reach statistical significance (p=0.11). Conclusion: Interleukin-10 knockout mice tend to develop more severe inflammation with endotoxin-induced uveitis at 24 hours than IL-10 competent mice. This lends support to the role of IL-10 as an anti-inflammatory cytokine. Although the germ free state should prevent exposure or tolerance to endotoxin, germ free mice in this study did not show a statistically significant increase in inflammation.

AB - Purpose: Interleukin-10 (IL-10) has been shown to inhibit inflammation seen with endotoxin-induced uveitis in mice and rabbits. We studied mice genetically deficient in IL10 to see if they have increased inflammation in response to intravitreal endotoxin. Methods: Germ free (GF) and conventional (nGF) C57BL/6 X 129 mice genetically deficient for the IL-10 gene (IL-10KO) and congenic littermates showing IL-10 expression (IL-10+) underwent intravitreal injection of 1 /d (trial 1) or 2 1 (trial 2) of 125ng//tl endotoxin in buffer. At 24 hours the mice were euthanized. Inflammation was graded by a masked observer who counted leukocytes in a cross-section of the eye. Result: In trial 1, eleven GF IL-10KO mice had a mean ±SE of 72+25 cells per section (cps). Twelve nGFIL-10KOmicehadameanof70±46cps. Ten nGF IL-10+ mice had a mean of 13+9 cps. The difference in inflammation seen between IL-10+ and IL-10KO mice was statistically significant (p=0.02). In trial 2, eleven GF IL-10KO mice had a mean of 761 ±147 cps. Seven nGF IL-10KO mice had a mean of 1365±360 cps. Five GF IL10+ mice had a mean of 384±81 cps. Two nGF IL-10+ mice had a mean of 731 ±9 cps. This trend for more inflammation in the IL-10KO group did not reach statistical significance (p=0.11). Conclusion: Interleukin-10 knockout mice tend to develop more severe inflammation with endotoxin-induced uveitis at 24 hours than IL-10 competent mice. This lends support to the role of IL-10 as an anti-inflammatory cytokine. Although the germ free state should prevent exposure or tolerance to endotoxin, germ free mice in this study did not show a statistically significant increase in inflammation.

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