Abstract

Lipopolysaccharide (LPS)-binding protein (LBP) functions as an acute phase protein and plays a key role in the innate immune response to bacterial challenge. It is a potential acute-phase biomarker in monitoring the progress of severe sepsis, infectious endocarditis and cardiovascular disease. LBP is mainly synthesized in hepatocytes and generates binding of bacteria and/or their products such as LPS to cell surface receptors, thereby initiating an innate host response. Interestingly, LBP has a dual role depending on its relatively low or high concentrations, and augments or downregulates the innate host defense accordingly. Emerging evidence indicates that LBP can be produced by non-hepatocytes, including respiratory type II epithelial cells, intestinal epithelial cells and human gingival epithelia. These findings suggest that LBP formation at extrahepatic cells may be crucial in containing microbial in situ challenge constantly, critically contributing to tissue homeostasis. This review provides an update on the characteristics and novel functions of LBP as well as its gene polymorphisms and potential use as a biomarker in assessing common infectious and inflammatory diseases such as periodontal disease. This paper highlights the expression profiles of LBP in human oral/gingival cells, how its expression could be modulated by periodontopathogens such as Porphyromonas gingivalis, as well as the relevant regulation mechanisms and signaling pathways involved. The critical roles of LBP in periodontal homeostasis and perspectives for its clinical application are discussed.

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