Endogenous MCP-1 promotes lung inflammation induced by LPS and LTA

Type of Publication: Journal article
Publication status: Published
Author: van Zoelen, Marieke A. D.; Verstege, Marleen I.; Draing, Christian; de Beer, Regina; van't Veer, Cornelis; Florquin, Sandrine; Bresser, Paul; Van der Zee, Jaring S.; te Velde, Anje A.; von Aulock, Sonja; van der Poll, Tom
Year of publication: 2011
Published in: Molecular Immunology ; 48 (2011), 12-13. - pp. 1468-1476. - Elsevier. - ISSN 0161-5890. - eISSN 1872-9142
Pubmed ID: 21529952
DOI (citable link): https://dx.doi.org/10.1016/j.molimm.2011.04.001
Summary:
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) 6 h 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-α 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.
Subject (DDC): 570 Biosciences, Biology
Keywords: Lung inflammation; Lipopolysaccharide; Lipoteichoic acid; Monocyte chemoattractant protein 1; Soluble receptor for advanced glycation end products; Animal models
Bibliography of Konstanz: Yes
Refereed: Yes

Cite This

Files in this item

Files Size Format View

There are no files associated with this item.

VAN ZOELEN, Marieke A. D., Marleen I. VERSTEGE, Christian DRAING, Regina DE BEER, Cornelis VAN'T VEER, Sandrine FLORQUIN, Paul BRESSER, Jaring S. VAN DER ZEE, Anje A. TE VELDE, Sonja VON AULOCK, Tom VAN DER POLL, 2011. Endogenous MCP-1 promotes lung inflammation induced by LPS and LTA. In: Molecular Immunology. Elsevier. 48(12-13), pp. 1468-1476. ISSN 0161-5890. eISSN 1872-9142. Available under: doi: 10.1016/j.molimm.2011.04.001

@article{vanZoelen2011-07Endog-51216, title={Endogenous MCP-1 promotes lung inflammation induced by LPS and LTA}, year={2011}, doi={10.1016/j.molimm.2011.04.001}, number={12-13}, volume={48}, issn={0161-5890}, journal={Molecular Immunology}, pages={1468--1476}, author={van Zoelen, Marieke A. D. and Verstege, Marleen I. and Draing, Christian and de Beer, Regina and van't Veer, Cornelis and Florquin, Sandrine and Bresser, Paul and Van der Zee, Jaring S. and te Velde, Anje A. and von Aulock, Sonja and van der Poll, Tom} }

Verstege, Marleen I. Endogenous MCP-1 promotes lung inflammation induced by LPS and LTA Van der Zee, Jaring S. Van der Zee, Jaring S. von Aulock, Sonja Verstege, Marleen I. de Beer, Regina van Zoelen, Marieke A. D. eng Draing, Christian 2020-10-06T09:00:53Z van't Veer, Cornelis von Aulock, Sonja Bresser, Paul te Velde, Anje A. Florquin, Sandrine van't Veer, Cornelis van der Poll, Tom van der Poll, Tom 2011-07 Florquin, Sandrine 2020-10-06T09:00:53Z Draing, Christian de Beer, Regina Bresser, Paul te Velde, Anje A. van Zoelen, Marieke A. D. 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) 6 h 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<sup>−/−</sup> mice demonstrated lower TNF-α levels and a diminished neutrophil influx into their bronchoalveolar space after either LPS or LTA instillation. After intrapulmonary delivery of LPS MCP-1<sup>−/−</sup> 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.

This item appears in the following Collection(s)

Search KOPS


Browse

My Account