PMID- 20584001
OWN - NLM
STAT- MEDLINE
DCOM- 20110419
LR  - 20110225
IS  - 1755-3768 (Electronic)
IS  - 1755-375X (Linking)
VI  - 89
IP  - 2
DP  - 2011 Mar
TI  - Neutrophil-dominant experimental autoimmune uveitis in CC-chemokine receptor 2 
      knockout mice.
PG  - e180-8
LID - 10.1111/j.1755-3768.2010.01953.x [doi]
AB  - PURPOSE: Murine experimental autoimmune uveitis (EAU) is an animal model of human 
      uveitis. It has been demonstrated that ocular-infiltrating macrophages are 
      crucial for EAU induction, and monocyte chemoattractant protein-1 (MCP-1) was 
      actually upregulated in the eye. CC chemokine receptor-2 (CCR2) is the receptor 
      of MCP-1, and macrophages fail to recruit particular lesions in CCR2 knockout 
      (KO) mice. To confirm the role of macrophages in EAU, we examined EAU in CCR2 KO 
      mice. METHODS: CCR2 KO mice and wild-type (WT) mice that had the same genetic 
      background were immunized with human interphotoreceptor retinoid-binding protein 
      peptide 1-20 emulsified in complete Freund's adjuvant. At multiple time-points, 
      EAU severity was evaluated based on microscopic fundus observation and 
      histological examination. To examine the phenotype of retinal-infiltrating cells, 
      single cells were prepared from the eye and analysed by flow cytometry. RESULTS: 
      In WT mice, EAU was induced at the peak of day 16 and marked macrophage 
      infiltration was observed. Although macrophages failed to be recruited into the 
      eye in CCR2 KO mice, severe uveitis was induced unexpectedly. Flow cytometry and 
      histology revealed that most of the infiltrating cells were neutrophils. We also 
      compared the intraocular chemokine concentrations between WT mice and KO mice. 
      Two CXC chemokine (monokine induced by interferon-gamma and interferon-gamma-inducible 
      protein-10) were upregulated in KO mice. CONCLUSION: Interphotoreceptor 
      retinoid-binding protein peptide immunization caused neutrophil-dominant uveitis 
      in CCR2 KO mice. In the absence of macrophages, neutrophils can be alternatively 
      recruited and can cause tissue damage.
CI  - (c) 2010 The Authors. Journal compilation (c) 2010 Acta Ophthalmol.
FAU - Sonoda, Koh-Hei
AU  - Sonoda KH
AD  - Department of Ophthalmology, Graduate School of Medical Science, Kyushu 
      University, Fukuoka, Japan. sonodak@med.kyushu-u.ac.jp
FAU - Yoshimura, Takeru
AU  - Yoshimura T
FAU - Egashira, Kensuke
AU  - Egashira K
FAU - Charo, Israel F
AU  - Charo IF
FAU - Ishibashi, Tatsuro
AU  - Ishibashi T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Acta Ophthalmol
JT  - Acta ophthalmologica
JID - 101468102
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Eye Proteins)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Retinol-Binding Proteins)
RN  - 0 (interstitial retinol-binding protein)
SB  - IM
MH  - Animals
MH  - Autoimmune Diseases/*immunology
MH  - Chemokine CCL2/immunology
MH  - Cytokines/immunology
MH  - *Disease Models, Animal
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Eye Proteins
MH  - Female
MH  - Flow Cytometry
MH  - Immunophenotyping
MH  - Macrophages/immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Neutrophils/*immunology
MH  - Receptors, CCR2/*physiology
MH  - Retinitis/immunology
MH  - Retinol-Binding Proteins
MH  - Th1 Cells/immunology
MH  - Uveitis, Posterior/*immunology
EDAT- 2010/06/30 06:00
MHDA- 2011/04/20 06:00
CRDT- 2010/06/30 06:00
PHST- 2010/06/30 06:00 [entrez]
PHST- 2010/06/30 06:00 [pubmed]
PHST- 2011/04/20 06:00 [medline]
AID - AOS1953 [pii]
AID - 10.1111/j.1755-3768.2010.01953.x [doi]
PST - ppublish
SO  - Acta Ophthalmol. 2011 Mar;89(2):e180-8. doi: 10.1111/j.1755-3768.2010.01953.x.