PMID- 10570305
OWN - NLM
STAT- MEDLINE
DCOM- 19991220
LR  - 20171116
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 163
IP  - 11
DP  - 1999 Dec 1
TI  - Endogenous monocyte chemoattractant protein-1 (MCP-1) protects mice in a model of 
      acute septic peritonitis: cross-talk between MCP-1 and leukotriene B4.
PG  - 6148-54
AB  - We investigated the involvement of monocyte chemoattractant protein (MCP)-1 in a 
      murine model of septic peritonitis induced by cecal ligation and puncture (CLP). 
      Initial studies demonstrated that CLP induced a dramatic increase in MCP-1 
      production in the peritoneum, followed by an increase in the recruitment of 
      leukocytes. MCP-1 blockade with anti-MCP-1 antiserum significantly decreased the 
      survival rate following CLP, which was accompanied by an enhanced recovery of 
      viable bacteria from the peritoneum. This was likely due to the reduction in the 
      recruitment and activation of both macrophages and neutrophils. To understand the 
      mechanisms whereby MCP-1 may influence neutrophil infiltration, levels of 
      chemokines known to attract neutrophils were monitored, which showed that 
      peritoneal levels of macrophage-inflammatory protein (MIP)-2, KC, and MIP-1alpha 
      were not altered with anti-MCP-1 Abs. However, anti-MCP-1 Abs reduced the 
      peritoneal levels of leukotriene B4 (LTB4) by 59%. The i.p. injection of MCP-1 
      into normal mice resulted in elevated levels of LTB4 in the peritoneum. In vitro, 
      MCP-1 stimulated the production of LTB4 from peritoneal macrophages, in a 
      dose-dependent manner. A specific LTB4 receptor antagonist (CP-105, 696) 
      inhibited CLP-induced recruitment of both neutrophils and macrophages, which was 
      accompanied by a reduced level of MCP-1 in the peritoneum. Finally, 
      administration of CP-105,696 was extremely detrimental to the survival of mice 
      following CLP. These experiments demonstrate that endogenous MCP-1 serves as an 
      indirect mediator to attract neutrophils via the production of LTB4, and suggest 
      the cross-talk can occur between MCP-1 and the lipid mediator LTB4 during septic 
      peritonitis.
FAU - Matsukawa, A
AU  - Matsukawa A
AD  - Departments ofPathology and Internal Medicine, Division of Pulmonary and Critical 
      Care, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
FAU - Hogaboam, C M
AU  - Hogaboam CM
FAU - Lukacs, N W
AU  - Lukacs NW
FAU - Lincoln, P M
AU  - Lincoln PM
FAU - Strieter, R M
AU  - Strieter RM
FAU - Kunkel, S L
AU  - Kunkel SL
LA  - eng
GR  - HL31237/HL/NHLBI NIH HHS/United States
GR  - P50HL60289/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Benzopyrans)
RN  - 0 (Carboxylic Acids)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Receptors, Leukotriene B4)
RN  - 1HGW4DR56D (Leukotriene B4)
RN  - Z7354TW4BM (CP 105696)
SB  - IM
MH  - Animals
MH  - Ascitic Fluid/chemistry
MH  - Benzopyrans/pharmacology
MH  - Carboxylic Acids/pharmacology
MH  - Cecum/surgery
MH  - Chemokine CCL2/blood/*metabolism
MH  - Chemokines/biosynthesis
MH  - Female
MH  - Leukotriene B4/*metabolism
MH  - Mice
MH  - Peritoneal Cavity/microbiology
MH  - Peritonitis/*immunology
MH  - *Receptor Cross-Talk
MH  - Receptors, Leukotriene B4/antagonists & inhibitors
MH  - Sepsis/*immunology
EDAT- 1999/11/26 00:00
MHDA- 1999/11/26 00:01
CRDT- 1999/11/26 00:00
PHST- 1999/11/26 00:00 [pubmed]
PHST- 1999/11/26 00:01 [medline]
PHST- 1999/11/26 00:00 [entrez]
AID - ji_v163n11p6148 [pii]
PST - ppublish
SO  - J Immunol. 1999 Dec 1;163(11):6148-54.