Effect of IL-10 antisense gene therapy in severely burned mice intradermally infected with MRSA

Akira Asai, Mari Kogiso, Makiko Kobayashi, David Herndon, Fujio Suzuki

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

The effect of IL-10 antisense oligodeoxynucleotides (ODN) on the susceptibility of burned mice to intradermal (i.d.) infection of methicillin-resistant Staphylococcus aureus (MRSA) was studied. Abscesses formed and sepsis did not develop in normal mice infected i.d. with 108CFU/mouse of MRSA. Similarly, sepsis caused by MRSA i.d. infection did not develop and abscesses formed in burned mice treated with IL-10 antisense ODN. However, all of the burned mice treated with scrambled ODN (control group) died by infectious complications stemming from MRSA i.d. infection, and an MRSA-abscess did not form in these mice. Macrophages (Mφ) isolated from the infection site tissue of burned mice that were treated with IL-10 antisense ODN were identified as M1Mφ, while Mφ isolated from burned mice that were treated with scrambled ODN were shown to be M2Mφ. MRSA-abscesses formed in burned mice inoculated with M1Mφ, and these mice resisted a lethal dose of MRSA i.d. infection. However, an abscess did not form, and sepsis caused by MRSA i.d. infection developed in burned mice that were inoculated with M2Mφ. These results indicate that severely burned mice treated with IL-10 antisense ODN are resistant against i.d. infection with MRSA. M1Mφ appeared in the infection site tissues of severely burned mice that were treated with IL-10 antisense ODN may play a role on the abscess formation and inhibiting sepsis caused by MRSA i.d. infection.

Original languageEnglish (US)
Pages (from-to)711-718
Number of pages8
JournalImmunobiology
Volume217
Issue number7
DOIs
StatePublished - Jul 2012

Fingerprint

Methicillin-Resistant Staphylococcus aureus
Genetic Therapy
Interleukin-10
Oligodeoxyribonucleotides
Abscess
Infection
Sepsis
Macrophages

Keywords

  • Immunosuppression
  • Macrophages
  • MRSA intradermal infection

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Hematology

Cite this

Effect of IL-10 antisense gene therapy in severely burned mice intradermally infected with MRSA. / Asai, Akira; Kogiso, Mari; Kobayashi, Makiko; Herndon, David; Suzuki, Fujio.

In: Immunobiology, Vol. 217, No. 7, 07.2012, p. 711-718.

Research output: Contribution to journalArticle

Asai, Akira ; Kogiso, Mari ; Kobayashi, Makiko ; Herndon, David ; Suzuki, Fujio. / Effect of IL-10 antisense gene therapy in severely burned mice intradermally infected with MRSA. In: Immunobiology. 2012 ; Vol. 217, No. 7. pp. 711-718.
@article{43f9a6d7c2864b0f987c093585f26e37,
title = "Effect of IL-10 antisense gene therapy in severely burned mice intradermally infected with MRSA",
abstract = "The effect of IL-10 antisense oligodeoxynucleotides (ODN) on the susceptibility of burned mice to intradermal (i.d.) infection of methicillin-resistant Staphylococcus aureus (MRSA) was studied. Abscesses formed and sepsis did not develop in normal mice infected i.d. with 108CFU/mouse of MRSA. Similarly, sepsis caused by MRSA i.d. infection did not develop and abscesses formed in burned mice treated with IL-10 antisense ODN. However, all of the burned mice treated with scrambled ODN (control group) died by infectious complications stemming from MRSA i.d. infection, and an MRSA-abscess did not form in these mice. Macrophages (Mφ) isolated from the infection site tissue of burned mice that were treated with IL-10 antisense ODN were identified as M1Mφ, while Mφ isolated from burned mice that were treated with scrambled ODN were shown to be M2Mφ. MRSA-abscesses formed in burned mice inoculated with M1Mφ, and these mice resisted a lethal dose of MRSA i.d. infection. However, an abscess did not form, and sepsis caused by MRSA i.d. infection developed in burned mice that were inoculated with M2Mφ. These results indicate that severely burned mice treated with IL-10 antisense ODN are resistant against i.d. infection with MRSA. M1Mφ appeared in the infection site tissues of severely burned mice that were treated with IL-10 antisense ODN may play a role on the abscess formation and inhibiting sepsis caused by MRSA i.d. infection.",
keywords = "Immunosuppression, Macrophages, MRSA intradermal infection",
author = "Akira Asai and Mari Kogiso and Makiko Kobayashi and David Herndon and Fujio Suzuki",
year = "2012",
month = "7",
doi = "10.1016/j.imbio.2011.12.002",
language = "English (US)",
volume = "217",
pages = "711--718",
journal = "Immunobiology",
issn = "0171-2985",
publisher = "Urban und Fischer Verlag GmbH und Co. KG",
number = "7",

}

TY - JOUR

T1 - Effect of IL-10 antisense gene therapy in severely burned mice intradermally infected with MRSA

AU - Asai, Akira

AU - Kogiso, Mari

AU - Kobayashi, Makiko

AU - Herndon, David

AU - Suzuki, Fujio

PY - 2012/7

Y1 - 2012/7

N2 - The effect of IL-10 antisense oligodeoxynucleotides (ODN) on the susceptibility of burned mice to intradermal (i.d.) infection of methicillin-resistant Staphylococcus aureus (MRSA) was studied. Abscesses formed and sepsis did not develop in normal mice infected i.d. with 108CFU/mouse of MRSA. Similarly, sepsis caused by MRSA i.d. infection did not develop and abscesses formed in burned mice treated with IL-10 antisense ODN. However, all of the burned mice treated with scrambled ODN (control group) died by infectious complications stemming from MRSA i.d. infection, and an MRSA-abscess did not form in these mice. Macrophages (Mφ) isolated from the infection site tissue of burned mice that were treated with IL-10 antisense ODN were identified as M1Mφ, while Mφ isolated from burned mice that were treated with scrambled ODN were shown to be M2Mφ. MRSA-abscesses formed in burned mice inoculated with M1Mφ, and these mice resisted a lethal dose of MRSA i.d. infection. However, an abscess did not form, and sepsis caused by MRSA i.d. infection developed in burned mice that were inoculated with M2Mφ. These results indicate that severely burned mice treated with IL-10 antisense ODN are resistant against i.d. infection with MRSA. M1Mφ appeared in the infection site tissues of severely burned mice that were treated with IL-10 antisense ODN may play a role on the abscess formation and inhibiting sepsis caused by MRSA i.d. infection.

AB - The effect of IL-10 antisense oligodeoxynucleotides (ODN) on the susceptibility of burned mice to intradermal (i.d.) infection of methicillin-resistant Staphylococcus aureus (MRSA) was studied. Abscesses formed and sepsis did not develop in normal mice infected i.d. with 108CFU/mouse of MRSA. Similarly, sepsis caused by MRSA i.d. infection did not develop and abscesses formed in burned mice treated with IL-10 antisense ODN. However, all of the burned mice treated with scrambled ODN (control group) died by infectious complications stemming from MRSA i.d. infection, and an MRSA-abscess did not form in these mice. Macrophages (Mφ) isolated from the infection site tissue of burned mice that were treated with IL-10 antisense ODN were identified as M1Mφ, while Mφ isolated from burned mice that were treated with scrambled ODN were shown to be M2Mφ. MRSA-abscesses formed in burned mice inoculated with M1Mφ, and these mice resisted a lethal dose of MRSA i.d. infection. However, an abscess did not form, and sepsis caused by MRSA i.d. infection developed in burned mice that were inoculated with M2Mφ. These results indicate that severely burned mice treated with IL-10 antisense ODN are resistant against i.d. infection with MRSA. M1Mφ appeared in the infection site tissues of severely burned mice that were treated with IL-10 antisense ODN may play a role on the abscess formation and inhibiting sepsis caused by MRSA i.d. infection.

KW - Immunosuppression

KW - Macrophages

KW - MRSA intradermal infection

UR - http://www.scopus.com/inward/record.url?scp=84861197671&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84861197671&partnerID=8YFLogxK

U2 - 10.1016/j.imbio.2011.12.002

DO - 10.1016/j.imbio.2011.12.002

M3 - Article

C2 - 22209112

AN - SCOPUS:84861197671

VL - 217

SP - 711

EP - 718

JO - Immunobiology

JF - Immunobiology

SN - 0171-2985

IS - 7

ER -