PMID- 9185504
OWN - NLM
STAT- MEDLINE
DCOM- 19970721
LR  - 20181113
IS  - 0021-9738 (Print)
IS  - 0021-9738 (Linking)
VI  - 99
IP  - 12
DP  - 1997 Jun 15
TI  - MCP-1 protects mice in lethal endotoxemia.
PG  - 2832-6
AB  - The overzealous production of proinflammatory cytokines in sepsis can result in 
      shock, multiorgan dysfunction, and even death. In this study, we assessed the 
      role of monocyte chemoattractant protein-1 (MCP-1) as a mediator of sepsis in 
      endotoxin-challenged mice. Intraperitoneal administration of LPS to CD-1 mice 
      induced a substantial time-dependent increase in MCP-1 in plasma, lung, and 
      liver. The passive immunization of mice with rabbit antimurine MCP-1 antiserum 2 
      h before endotoxin administration resulted in a striking increase in LPS-induced 
      mortality from 10% in control animals to 65% in anti-MCP-1-treated animals. 
      Importantly, the administration of anti-MCP-1 antibodies to endotoxin-challenged 
      mice resulted in increases in peak TNF-alpha and IL-12 levels, and also in a 
      trend toward decreased serum levels of IL-10. Conversely, the administration of 
      recombinant murine MCP-1 intraperitoneally significantly protected mice from 
      endotoxin-induced lethality, and resulted in an increase in IL-10 levels, a 
      decrease in IL-12 levels, and a trend toward decreased levels of TNF. In 
      conclusion, our findings indicate that MCP-1 is a protective cytokine expressed 
      in murine endotoxemia, and does so by shifting the balance in favor of 
      antiinflammatory cytokine expression in endotoxin-challenged animals.
FAU - Zisman, D A
AU  - Zisman DA
AD  - Department of Medicine, Division of Pulmonary and Critical Care Medicine, The 
      University of Michigan Medical School, Ann Arbor, Michigan 48109-0360, USA.
FAU - Kunkel, S L
AU  - Kunkel SL
FAU - Strieter, R M
AU  - Strieter RM
FAU - Tsai, W C
AU  - Tsai WC
FAU - Bucknell, K
AU  - Bucknell K
FAU - Wilkowski, J
AU  - Wilkowski J
FAU - Standiford, T J
AU  - Standiford TJ
LA  - eng
GR  - HL35276/HL/NHLBI NIH HHS/United States
GR  - HL50057/HL/NHLBI NIH HHS/United States
GR  - HL58200/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Clin Invest
JT  - The Journal of clinical investigation
JID - 7802877
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
RN  - 187348-17-0 (Interleukin-12)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/immunology/*physiology/therapeutic use
MH  - Endotoxemia/mortality/*prevention & control
MH  - Female
MH  - Immunization, Passive
MH  - Interleukin-10/blood
MH  - Interleukin-12/blood
MH  - Kinetics
MH  - Lipopolysaccharides/administration & dosage
MH  - Mice
MH  - Recombinant Proteins/therapeutic use
MH  - Tumor Necrosis Factor-alpha/metabolism
PMC - PMC508132
EDAT- 1997/06/15 00:00
MHDA- 1997/06/15 00:01
PMCR- 1997/06/15
CRDT- 1997/06/15 00:00
PHST- 1997/06/15 00:00 [pubmed]
PHST- 1997/06/15 00:01 [medline]
PHST- 1997/06/15 00:00 [entrez]
PHST- 1997/06/15 00:00 [pmc-release]
AID - 10.1172/JCI119475 [doi]
PST - ppublish
SO  - J Clin Invest. 1997 Jun 15;99(12):2832-6. doi: 10.1172/JCI119475.