PMID- 11567658
OWN - NLM
STAT- MEDLINE
DCOM- 20011101
LR  - 20190624
IS  - 0014-2999 (Print)
IS  - 0014-2999 (Linking)
VI  - 427
IP  - 3
DP  - 2001 Sep 21
TI  - Redundant function of macrophage inflammatory protein-2 and KC in tumor necrosis 
      factor-alpha-induced extravasation of neutrophils in vivo.
PG  - 277-83
AB  - Tumor necrosis factor-alpha (TNF-alpha) stimulates the expression CXC chemokines, 
      i.e. macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil 
      chemoattractant (KC), and neutrophil extravasation. However, the individual role 
      of MIP-2 and KC in the recruitment process of neutrophils in vivo remains 
      elusive. By use of intravital microscopy in the mouse cremaster muscle, we 
      analyzed the effect of specific inhibition of CXC chemokines, alone and together, 
      on TNF-alpha-induced leukocyte rolling, firm adhesion and recruitment. After 
      stimulation with TNF-alpha, the mRNA levels of both MIP-2 and KC were increased. 
      Notably, separate administration of antibodies directed against MIP-2 and KC had 
      no effect on TNF-alpha-induced neutrophil extravasation. In contrast, combined 
      injection of anti-MIP-2 and anti-KC antibodies markedly inhibited extravascular 
      migration of neutrophils. Moreover, MIP-2 and KC dose-dependently increased 
      neutrophil recruitment, however, no synergistic effect of combined stimulation 
      with MIP-2 and KC on the neutrophil response was found. Taken together, these 
      data suggest that MIP-2 and KC are functionally redundant in TNF-alpha-induced 
      neutrophil accumulation and that neutralization of both MIP-2 and KC may be 
      necessary in order to reduce accumulation of neutrophils in cytokine-activated 
      tissues.
FAU - Zhang, X W
AU  - Zhang XW
AD  - Department of Surgery, Malmo University Hospital, Lund University, 20502 Malmo, 
      Sweden.
FAU - Wang, Y
AU  - Wang Y
FAU - Liu, Q
AU  - Liu Q
FAU - Thorlacius, H
AU  - Thorlacius H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Chemokine CXCL2)
RN  - 0 (Chemokines)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Cxcl2 protein, mouse)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/pharmacology
MH  - Blood Flow Velocity/drug effects
MH  - Capillary Permeability/drug effects
MH  - Chemokine CXCL2
MH  - Chemokines/genetics/immunology/*pharmacology
MH  - Chemotactic Factors/genetics/immunology/*pharmacology
MH  - Chemotaxis, Leukocyte/drug effects
MH  - Dose-Response Relationship, Drug
MH  - Erythrocytes/drug effects/physiology
MH  - Gene Expression Regulation/drug effects
MH  - Leukocyte Count
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Muscle, Skeletal/blood supply/drug effects/metabolism
MH  - Neutrophil Infiltration/drug effects
MH  - Neutrophils/cytology/*drug effects
MH  - RNA, Messenger/drug effects/genetics/metabolism
MH  - Rats
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 2001/09/25 10:00
MHDA- 2001/11/03 10:01
CRDT- 2001/09/25 10:00
PHST- 2001/09/25 10:00 [pubmed]
PHST- 2001/11/03 10:01 [medline]
PHST- 2001/09/25 10:00 [entrez]
AID - S0014299901012353 [pii]
AID - 10.1016/s0014-2999(01)01235-3 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2001 Sep 21;427(3):277-83. doi: 10.1016/s0014-2999(01)01235-3.