PMID- 21529952
OWN - NLM
STAT- MEDLINE
DCOM- 20110810
LR  - 20220414
IS  - 1872-9142 (Electronic)
IS  - 0161-5890 (Linking)
VI  - 48
IP  - 12-13
DP  - 2011 Jul
TI  - Endogenous MCP-1 promotes lung inflammation induced by LPS and LTA.
PG  - 1468-76
LID - 10.1016/j.molimm.2011.04.001 [doi]
AB  - Monocyte chemoattractant protein 1 (MCP-1) plays an important role in leukocyte 
      recruitment to sites of infection and inflammation. In addition, MCP-1 may 
      attenuate inflammation by virtue of its capacity to inhibit the production of 
      proinflammatory cytokines. We here investigated the role of MCP-1 in lung 
      inflammation induced by lipopolysaccharide (LPS) or lipoteichoic acid (LTA), 
      constituents of the gram-negative and gram-positive bacterial cell wall, 
      respectively. Healthy humans demonstrated elevated MCP-1 concentrations in their 
      bronchoalveolar lavage fluid (BALF) 6h after inhalation of LPS. Similarly, 
      intranasal administration of LPS or LTA to mice resulted in a rise in BALF MCP-1 
      levels. Murine alveolar macrophage-like cells released significant amounts of 
      MCP-1 upon stimulation with LPS or LTA in vitro. Compared to Wt mice, MCP-1(-/-) 
      mice demonstrated lower TNF-alpha levels and a diminished neutrophil influx into 
      their bronchoalveolar space after either LPS or LTA instillation. After 
      intrapulmonary delivery of LPS MCP-1(-/-) mice had decreased interleukin-6 and KC 
      concentrations and less severe lung inflammation upon histopathological 
      examination. Remarkably, MCP-1 deficiency was associated with an early 
      enhancement of interleukin-10 release in BALF after both LPS and LTA 
      instillation. These data suggest that MCP-1 is a proinflammatory mediator during 
      pulmonary inflammation induced by either LPS or LTA.
CI  - Copyright (c) 2011 Elsevier Ltd. All rights reserved.
FAU - van Zoelen, Marieke A D
AU  - van Zoelen MA
AD  - Center for Infection and Immunity Amsterdam, Academic Medical Center, 
      Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. M.A.vanZoelen@amc.uva.nl
FAU - Verstege, Marleen I
AU  - Verstege MI
FAU - Draing, Christian
AU  - Draing C
FAU - de Beer, Regina
AU  - de Beer R
FAU - van't Veer, Cornelis
AU  - van't Veer C
FAU - Florquin, Sandrine
AU  - Florquin S
FAU - Bresser, Paul
AU  - Bresser P
FAU - van der Zee, Jaring S
AU  - van der Zee JS
FAU - te Velde, Anje A
AU  - te Velde AA
FAU - von Aulock, Sonja
AU  - von Aulock S
FAU - van der Poll, Tom
AU  - van der Poll T
LA  - eng
PT  - Journal Article
DEP - 20110506
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Teichoic Acids)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 130068-27-8 (Interleukin-10)
RN  - 56411-57-5 (lipoteichoic acid)
SB  - IM
MH  - Animals
MH  - Bronchoalveolar Lavage Fluid/chemistry
MH  - Cell Count
MH  - Chemokine CCL2/deficiency/*physiology
MH  - Chemotaxis, Leukocyte
MH  - Cytokines/biosynthesis/immunology/metabolism
MH  - Female
MH  - Humans
MH  - Interleukin-10/blood
MH  - Interleukin-6/blood
MH  - Lipopolysaccharides/*immunology
MH  - Lung/*immunology
MH  - Macrophages, Alveolar/immunology/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Neutrophils/immunology
MH  - Pneumonia/*immunology
MH  - Teichoic Acids/*immunology
MH  - Tumor Necrosis Factor-alpha/blood
MH  - Young Adult
EDAT- 2011/05/03 06:00
MHDA- 2011/08/11 06:00
CRDT- 2011/05/03 06:00
PHST- 2010/01/04 00:00 [received]
PHST- 2011/03/28 00:00 [revised]
PHST- 2011/04/01 00:00 [accepted]
PHST- 2011/05/03 06:00 [entrez]
PHST- 2011/05/03 06:00 [pubmed]
PHST- 2011/08/11 06:00 [medline]
AID - S0161-5890(11)00118-0 [pii]
AID - 10.1016/j.molimm.2011.04.001 [doi]
PST - ppublish
SO  - Mol Immunol. 2011 Jul;48(12-13):1468-76. doi: 10.1016/j.molimm.2011.04.001. Epub 
      2011 May 6.