PMID- 16997857
OWN - NLM
STAT- MEDLINE
DCOM- 20070118
LR  - 20171116
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 80
IP  - 6
DP  - 2006 Dec
TI  - Depletion of MCP-1 increases development of herpetic stromal keratitis by innate 
      immune modulation.
PG  - 1405-15
AB  - Chemokines are important chemoattractant inflammatory molecules, but their 
      interdependent network in disease pathogenesis remains unclear. Studies in mouse 
      models have shown that herpetic stromal keratitis (SK) is produced by the 
      consequence of a tissue-destructive immunoinflammatory reaction involving herpes 
      simplex virus type 1 (HSV) infection. Here we found that ocular HSV infection 
      leads to increased expression of monocyte chemoattractant protein-1 (MCP-1), one 
      of the major chemoattractants for immune cells that express CCR2, in the SK 
      cornea. However, MCP-1 is unlikely to be a chemoattractant for infiltrating 
      Gr-1(+), CD11b(+) cells in SK, as these cells are found to be CCR2 negative. 
      Nevertheless, infection of MCP-1(-/-) mice resulted in more severe SK lesion 
      severity compared with WT mice (P<0.01). We demonstrated that the loss of MCP-1 
      in the SK cornea caused a significant overexpression of macrophage inflammatory 
      protein-2 (MIP-2) (P<0.01) on days 2 and 4 postinfection and increased 
      infiltration of inflammatory cells (Gr-1-high and CD11b(+)) expressing CXCR2, a 
      receptor for MIP-2, into the cornea. Subsequently, increased infiltration of 
      inflammatory cells accelerated by MIP-2 overexpression might result in the high 
      production of inflammatory molecules, including vascular endothelial growth 
      factor (VEGF) and IL-1beta in SK, as well as CpG oligodeoxynucleotide 
      (ODN)-implanted eyes of MCP-1(-/-) mice. These results indicate that MCP-1 in the 
      SK cornea might regulate the expression of other chemokines, as well as the 
      infiltration of inflammatory cells and control development of SK.
FAU - Kim, Bumseok
AU  - Kim B
AD  - Department of Microbiology and Pathobiology, College of Veterinary Medicine, 
      University of Tennessee, Knoxville, TN 37996-0845, USA.
FAU - Sarangi, Pranita P
AU  - Sarangi PP
FAU - Lee, Yunsang
AU  - Lee Y
FAU - Deshpande Kaistha, Shilpa
AU  - Deshpande Kaistha S
FAU - Lee, Sujin
AU  - Lee S
FAU - Rouse, Barry T
AU  - Rouse BT
LA  - eng
GR  - R01 EY05093/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20060922
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (CCR2 protein, human)
RN  - 0 (CD11b Antigen)
RN  - 0 (Ccr2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL2)
RN  - 0 (Chemokines)
RN  - 0 (Cxcl2 protein, mouse)
RN  - 0 (Gr-1 protein, mouse)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Oligonucleotides)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, Chemokine)
SB  - IM
MH  - Animals
MH  - CD11b Antigen/immunology
MH  - Chemokine CCL2/deficiency/*immunology/metabolism
MH  - Chemokine CXCL2
MH  - Chemokines/biosynthesis/*immunology
MH  - Cornea/immunology/metabolism/virology
MH  - CpG Islands/immunology
MH  - Gene Expression Regulation/genetics/*immunology
MH  - Herpesvirus 1, Human/*immunology/metabolism
MH  - Inflammation/genetics/immunology/metabolism/virology
MH  - Interleukin-1beta/biosynthesis/immunology
MH  - Keratitis, Herpetic/genetics/*immunology/metabolism/virology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Oligonucleotides/immunology/pharmacology
MH  - Receptors, CCR2
MH  - Receptors, Chemokine/immunology/metabolism
MH  - Time Factors
EDAT- 2006/09/26 09:00
MHDA- 2007/01/19 09:00
CRDT- 2006/09/26 09:00
PHST- 2006/09/26 09:00 [pubmed]
PHST- 2007/01/19 09:00 [medline]
PHST- 2006/09/26 09:00 [entrez]
AID - jlb.0406295 [pii]
AID - 10.1189/jlb.0406295 [doi]
PST - ppublish
SO  - J Leukoc Biol. 2006 Dec;80(6):1405-15. doi: 10.1189/jlb.0406295. Epub 2006 Sep 
      22.