Objective   To investigate the possible mechanisms of traumatic infection-related inflammation via the pattern recognition receptors (PRRs) in innate immunocytes and provide the new idea for the measures in modulation of the excessive inflammatory responses.   Methods   The models of endotoxemic mice

cecal ligation and puncture

and immmunostimulated alveolar macrophages were used for the assay of PRRs by immunohistochemistry and reverse transcription PCR method. HEK293 cells co-transfected plasmids expressing CD14

TLR4 and MD-2 or two of them were stimulated with lipopolysaccharide (LPS) at the dose of 100 ng/ml for the determination of NF-κB and tumor necrosis factor (TNF)-α.   Results   SR was up-regulated while the expressions of CD14

TLR4 and MD-2 were down-regulated in innate immunocytes. The HEK293 cells co-transfected three types of plasmids enhanced the sensitivity to LPS binding and stimulation as compared with HEK293 cells co-transfected two of them (P0.05)

followed with the significant translocation of NF-κB and TNF-α secretion (P0.05).   Conclusion   Our data strongly indicate that the significant correlation between uncontrolled inflammatory responses and the imbalance between defensive receptors and effector receptors. The strategy of moderate regulation of PRRs can be a promising strategy in immunomodulation of inflammatory injuries.