کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2831234 | 1570736 | 2011 | 9 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Endogenous MCP-1 promotes lung inflammation induced by LPS and LTA Endogenous MCP-1 promotes lung inflammation induced by LPS and LTA](/preview/png/2831234.png)
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.
► MCP-1 is increased in BALF from healthy human volunteers after inhalation of LPS.
► In mice, MCP-1 deficiency was associated with lower TNF alpha levels and a declined neutrophil influx into the bronchoalveolar space after either LPS or LTA instillation.
► Intrapulmonary administration of LPS in MCP-1 deficient mice led to diminished IL-6 and KC concentrations and less severe lung injury.
► These data suggest that MCP-1 is a proinflammatory mediator during pulmonary inflammation induced by either LPS or LTA.
Journal: Molecular Immunology - Volume 48, Issues 12–13, July 2011, Pages 1468–1476