PMID- 20051242
OWN - NLM
STAT- MEDLINE
DCOM- 20100312
LR  - 20171116
IS  - 1090-2430 (Electronic)
IS  - 0014-4886 (Linking)
VI  - 222
IP  - 1
DP  - 2010 Mar
TI  - Deficiency of the negative immune regulator B7-H1 enhances inflammation and 
      neuropathic pain after chronic constriction injury of mouse sciatic nerve.
PG  - 153-60
LID - 10.1016/j.expneurol.2009.12.026 [doi]
AB  - Peripheral nerve injury induces a profound local inflammatory response that 
      involves T cells and macrophages and augments the generation of neuropathic pain. 
      The mechanisms underlying immune cell activation or inhibition in the peripheral 
      nervous system, however, are unknown. The co-inhibitory molecule B7-H1 (PD-L1, 
      CD274) attenuates immune cell proliferation and cytokine production and protects 
      from inflammation-induced tissue damage. We analyzed the temporal gene expression 
      profile of B7-H1 and different cytokines after chronic constriction injury (CCI) 
      of the sciatic nerve, a lesion paradigm inducing neuropathic pain, by 
      quantitative real-time polymerase chain reaction and immunohistochemistry in 
      B7-H1(-/-) mice and wild-type (WT) controls. B7-H1 mRNA was markedly induced in 
      WT nerves after CCI, and macrophages could be identified as major B7-H1 source. 
      The proinflammatory mediators tumor necrosis factor alpha (TNFalpha) and monocyte 
      chemoattractant protein-1 (MCP-1) displayed a strong, but transient expression in 
      degenerating nerves on day 1 after CCI in WT mice, while a biphasic expression 
      peak on day 1 and day 28 was found in B7-H1(-/-) mice. Overall, TNFalpha and 
      MCP-1 levels in B7-H1-deficient nerves dramatically exceeded those in WT 
      controls. In contrast, induction of the anti-inflammatory cytokine 
      interleukin(IL)-10 was restricted to WT nerves. The observation that B7-H1 
      deficiency enhances inflammation upon CCI was further corroborated by 
      immunohistochemistry showing increased numbers of T cells and macrophages in 
      injured nerves from B7-H1(-/-) mice. Interestingly, mechanical hyperalgesia was 
      more pronounced in the absence of B7-H1. Our study identifies B7-H1 as an 
      important suppressor of the inflammatory response and neuropathic pain occurring 
      after peripheral nerve injury.
CI  - Copyright 2009 Elsevier Inc. All rights reserved.
FAU - Uceyler, Nurcan
AU  - Uceyler N
AD  - Department of Neurology, University of Wurzburg, Josef-Schneider-Str. 11, 97080 
      Wurzburg, Germany.
FAU - Gobel, Kerstin
AU  - Gobel K
FAU - Meuth, Sven G
AU  - Meuth SG
FAU - Ortler, Sonja
AU  - Ortler S
FAU - Stoll, Guido
AU  - Stoll G
FAU - Sommer, Claudia
AU  - Sommer C
FAU - Wiendl, Heinz
AU  - Wiendl H
FAU - Kleinschnitz, Christoph
AU  - Kleinschnitz C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100104
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (B7-1 Antigen)
RN  - 0 (B7-H1 Antigen)
RN  - 0 (CD11b Antigen)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Cd274 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Peptides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - B7-1 Antigen
MH  - B7-H1 Antigen
MH  - CD11b Antigen/metabolism
MH  - Chemokine CCL2/genetics/metabolism
MH  - Constriction
MH  - Gene Expression Regulation/*genetics
MH  - Hyperalgesia/etiology/genetics
MH  - Interleukin-10/metabolism
MH  - Macrophages/metabolism
MH  - Male
MH  - Membrane Glycoproteins/*deficiency
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Pain Measurement/methods
MH  - Pain Threshold/physiology
MH  - Peptides/*deficiency
MH  - Physical Stimulation/methods
MH  - Sciatic Neuropathy/*immunology/*metabolism/physiopathology
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/genetics/metabolism
EDAT- 2010/01/07 06:00
MHDA- 2010/03/13 06:00
CRDT- 2010/01/07 06:00
PHST- 2009/10/19 00:00 [received]
PHST- 2009/12/17 00:00 [revised]
PHST- 2009/12/23 00:00 [accepted]
PHST- 2010/01/07 06:00 [entrez]
PHST- 2010/01/07 06:00 [pubmed]
PHST- 2010/03/13 06:00 [medline]
AID - S0014-4886(09)00519-6 [pii]
AID - 10.1016/j.expneurol.2009.12.026 [doi]
PST - ppublish
SO  - Exp Neurol. 2010 Mar;222(1):153-60. doi: 10.1016/j.expneurol.2009.12.026. Epub 
      2010 Jan 4.