Abstract
Abstract Dynamic polarizations of innate leukocytes such as monocytes and macrophages have been increasingly recognized to play key roles in the pathogenesis and/or treatment of human disease. However, mechanisms responsible for distinct polarizations of monocytes are not well understood. Our previous studies indicate that monocytes can be persistently polarized into a low-grade inflammatory state by subclinical super-low dose LPS (bacterial lipopolysaccharide). In this current study, we further characterized the unique polarization of monocytes by super-low dose LPS and its underlying mechanisms. We observed that super-low dose LPS preferentially induced the expression of inflammatory mediators such as MCP-1 while potently suppressed the expression of homeostatic mediators such as Catalase and FPN. Super-low dose LPS activated the inflammatory signaling molecules such as p38, CamKII, and NFkB. In contrast, super-low dose LPS suppressed the basal activation of immune suppressing molecules such as AMPK and SIRT3. Taken together, our data reveal novel insights regarding the persistent polarization of inflammatory monocyte, an emerging key player in various human diseases including cancer. Citation Format: Kisha Pradhan. Mechanisms responsible for the inflammatory polarization of monocytes by subclinical low-dose LPS [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4311.
Published Version
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