Macrophage polarization and MRSA infection in burned mice

Tomoki Nishiguchi, Ichiaki Ito, Jong Lee, Sumihiro Suzuki, Fujio Suzuki, Makiko Kobayashi

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Mortality associated with Staphylococcus aureus infection remains high during the sub-acute phase of burn injury. In this study, we aimed to improve antibacterial resistance of sub-acutely burned mice through macrophage polarization. Sepsis did not develop in mice at the sub-acute phase of 5% total body surface area (TBSA) burn after being infected with methicillin-resistant S. aureus (MRSA), and M1 macrophages (interleukin (IL)-10-IL-12+ inducible nitric oxide synthase+ Mφ) were isolated from these mice. In contrast, predominantly M2b macrophages (C-C motif chemokine ligand 1 (CCL1)+IL-10+IL-12- Mφ) were isolated from mice with >15% TBSA burn, and all of these mice died after the same MRSA infection. Comparing NOD scid gamma mice inoculated with Mφ with 25% TBSA burns, all mice treated with CCL1 antisense oligodeoxynucleotide (ODN) survived after MRSA infection, whereas all untreated mice given the same infection died within 4 days. CCL1 antisense ODN has been characterized as a specific polarizer of M2bMφ. M1Mφ were isolated from MRSA-infected mice with 25% TBSA burn after treatment with CCL1 antisense ODN, and these mice were shown to be resistant against a lethal dose of MRSA infection. M1Mφ were also isolated from 25% TBSA-burned mice infected with MRSA when the ODN was administered therapeutically, and subsequent sepsis was effectively controlled in these mice. These results indicate that the M2bMφ polarizer is beneficial for controlling MRSA infection in mice at the sub-acute phase of severe burn injury.Immunology and Cell Biology advance online publication, 15 November 2016; doi:10.1038/icb.2016.84.

Original languageEnglish (US)
JournalImmunology and Cell Biology
DOIs
StateAccepted/In press - Nov 15 2016

Fingerprint

Methicillin-Resistant Staphylococcus aureus
Macrophages
Infection
Body Surface Area
CC Chemokines
Oligodeoxyribonucleotides
Ligands
Interleukin-12
Interleukin-10
Sepsis
Wounds and Injuries
Nitric Oxide Synthase Type II
Allergy and Immunology
Burns
Cell Biology
Staphylococcus aureus
Publications

ASJC Scopus subject areas

  • Immunology
  • Cell Biology

Cite this

Macrophage polarization and MRSA infection in burned mice. / Nishiguchi, Tomoki; Ito, Ichiaki; Lee, Jong; Suzuki, Sumihiro; Suzuki, Fujio; Kobayashi, Makiko.

In: Immunology and Cell Biology, 15.11.2016.

Research output: Contribution to journalArticle

@article{a075687948f6412bb249a51aeebc1530,
title = "Macrophage polarization and MRSA infection in burned mice",
abstract = "Mortality associated with Staphylococcus aureus infection remains high during the sub-acute phase of burn injury. In this study, we aimed to improve antibacterial resistance of sub-acutely burned mice through macrophage polarization. Sepsis did not develop in mice at the sub-acute phase of 5{\%} total body surface area (TBSA) burn after being infected with methicillin-resistant S. aureus (MRSA), and M1 macrophages (interleukin (IL)-10-IL-12+ inducible nitric oxide synthase+ Mφ) were isolated from these mice. In contrast, predominantly M2b macrophages (C-C motif chemokine ligand 1 (CCL1)+IL-10+IL-12- Mφ) were isolated from mice with >15{\%} TBSA burn, and all of these mice died after the same MRSA infection. Comparing NOD scid gamma mice inoculated with Mφ with 25{\%} TBSA burns, all mice treated with CCL1 antisense oligodeoxynucleotide (ODN) survived after MRSA infection, whereas all untreated mice given the same infection died within 4 days. CCL1 antisense ODN has been characterized as a specific polarizer of M2bMφ. M1Mφ were isolated from MRSA-infected mice with 25{\%} TBSA burn after treatment with CCL1 antisense ODN, and these mice were shown to be resistant against a lethal dose of MRSA infection. M1Mφ were also isolated from 25{\%} TBSA-burned mice infected with MRSA when the ODN was administered therapeutically, and subsequent sepsis was effectively controlled in these mice. These results indicate that the M2bMφ polarizer is beneficial for controlling MRSA infection in mice at the sub-acute phase of severe burn injury.Immunology and Cell Biology advance online publication, 15 November 2016; doi:10.1038/icb.2016.84.",
author = "Tomoki Nishiguchi and Ichiaki Ito and Jong Lee and Sumihiro Suzuki and Fujio Suzuki and Makiko Kobayashi",
year = "2016",
month = "11",
day = "15",
doi = "10.1038/icb.2016.84",
language = "English (US)",
journal = "Immunology and Cell Biology",
issn = "0818-9641",
publisher = "Nature Publishing Group",

}

TY - JOUR

T1 - Macrophage polarization and MRSA infection in burned mice

AU - Nishiguchi, Tomoki

AU - Ito, Ichiaki

AU - Lee, Jong

AU - Suzuki, Sumihiro

AU - Suzuki, Fujio

AU - Kobayashi, Makiko

PY - 2016/11/15

Y1 - 2016/11/15

N2 - Mortality associated with Staphylococcus aureus infection remains high during the sub-acute phase of burn injury. In this study, we aimed to improve antibacterial resistance of sub-acutely burned mice through macrophage polarization. Sepsis did not develop in mice at the sub-acute phase of 5% total body surface area (TBSA) burn after being infected with methicillin-resistant S. aureus (MRSA), and M1 macrophages (interleukin (IL)-10-IL-12+ inducible nitric oxide synthase+ Mφ) were isolated from these mice. In contrast, predominantly M2b macrophages (C-C motif chemokine ligand 1 (CCL1)+IL-10+IL-12- Mφ) were isolated from mice with >15% TBSA burn, and all of these mice died after the same MRSA infection. Comparing NOD scid gamma mice inoculated with Mφ with 25% TBSA burns, all mice treated with CCL1 antisense oligodeoxynucleotide (ODN) survived after MRSA infection, whereas all untreated mice given the same infection died within 4 days. CCL1 antisense ODN has been characterized as a specific polarizer of M2bMφ. M1Mφ were isolated from MRSA-infected mice with 25% TBSA burn after treatment with CCL1 antisense ODN, and these mice were shown to be resistant against a lethal dose of MRSA infection. M1Mφ were also isolated from 25% TBSA-burned mice infected with MRSA when the ODN was administered therapeutically, and subsequent sepsis was effectively controlled in these mice. These results indicate that the M2bMφ polarizer is beneficial for controlling MRSA infection in mice at the sub-acute phase of severe burn injury.Immunology and Cell Biology advance online publication, 15 November 2016; doi:10.1038/icb.2016.84.

AB - Mortality associated with Staphylococcus aureus infection remains high during the sub-acute phase of burn injury. In this study, we aimed to improve antibacterial resistance of sub-acutely burned mice through macrophage polarization. Sepsis did not develop in mice at the sub-acute phase of 5% total body surface area (TBSA) burn after being infected with methicillin-resistant S. aureus (MRSA), and M1 macrophages (interleukin (IL)-10-IL-12+ inducible nitric oxide synthase+ Mφ) were isolated from these mice. In contrast, predominantly M2b macrophages (C-C motif chemokine ligand 1 (CCL1)+IL-10+IL-12- Mφ) were isolated from mice with >15% TBSA burn, and all of these mice died after the same MRSA infection. Comparing NOD scid gamma mice inoculated with Mφ with 25% TBSA burns, all mice treated with CCL1 antisense oligodeoxynucleotide (ODN) survived after MRSA infection, whereas all untreated mice given the same infection died within 4 days. CCL1 antisense ODN has been characterized as a specific polarizer of M2bMφ. M1Mφ were isolated from MRSA-infected mice with 25% TBSA burn after treatment with CCL1 antisense ODN, and these mice were shown to be resistant against a lethal dose of MRSA infection. M1Mφ were also isolated from 25% TBSA-burned mice infected with MRSA when the ODN was administered therapeutically, and subsequent sepsis was effectively controlled in these mice. These results indicate that the M2bMφ polarizer is beneficial for controlling MRSA infection in mice at the sub-acute phase of severe burn injury.Immunology and Cell Biology advance online publication, 15 November 2016; doi:10.1038/icb.2016.84.

UR - http://www.scopus.com/inward/record.url?scp=84995494419&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84995494419&partnerID=8YFLogxK

U2 - 10.1038/icb.2016.84

DO - 10.1038/icb.2016.84

M3 - Article

C2 - 27596946

AN - SCOPUS:84995494419

JO - Immunology and Cell Biology

JF - Immunology and Cell Biology

SN - 0818-9641

ER -