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Exp Mol Pathol. 2012 Dec;93(3):319-23. doi: 10.1016/j.yexmp.2012.08.006. Epub 2012 Sep 6.

Fingerprinting of the TLR4-induced acute inflammatory response.

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Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109-5602, USA.


Intensive scientific efforts in the past decades have helped shed light into the pathogenesis of endotoxin-induced inflammation. We have used multiplexing bead-based assays to characterize the responses in two models of in vivo LPS challenge. C57BL/6 mice were either injected intraperitoneally (endotoxemia) or intratracheally (acute lung injury; ALI) with lipopolysaccharide (LPS). The time courses (1h-24h) of the following 20 inflammatory mediators in plasma or broncho-alveolar lavages were simultaneously analyzed: IL-1α, IL-1β, IL-2, IL-3, IL-4, IL-5, IL-6, IL-9, IL-12(p40), IL-13, Eotaxin (CCL11), G-CSF, GM-CSF, IFN-γ, KC (CXCL1), MCP-1 (CCL2), MIP-1α (CCL3), MIP-1β (CCL4), RANTES (CCL5) and TNF-α. While significant inductions of all mediators were found, substantial differences in their absolute concentrations, time points of maximal concentrations and clearances were observed. There were also notable variations in the patterns of several cytokines/chemokines when samples from endotoxemia and LPS-ALI were compared. These data may be helpful in defining analytic strategies including selection of optimal time points for studying the host immune response to endotoxin.

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