Lipopolysaccharide Influences Adipokine Expression in 3T3-L1 Adipocytes.

Mediators Inflamm

Department of Microbiology and Immunology, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi, Tokyo 173-8605, Japan.

Published: May 2018

AI Article Synopsis

  • The text discusses the link between a specific opportunistic pathogen and an increased risk of hospital-acquired infections in obese individuals, suggesting a potential interaction with white adipose tissue.
  • The study focuses on how lipopolysaccharides (LPS) derived from the pathogen affect adipocyte functionality, particularly using the 3T3-L1 cell line as a model.
  • Results showed that LPS exposure increased several inflammatory adipokines while reducing levels of leptin and adiponectin, indicating that LPS could play a role in the inflammatory response of white adipose tissue at a molecular level.

Article Abstract

is one of the most important nosocomial opportunistic pathogen worldwide. In addition, obesity has been associated with an increased risk of nosocomial infection, suggesting that there may be an association between and white adipose tissue. However, the effects of on adipocytes have not been well studied at the molecular level. Here, we investigated the potential role of -derived lipopolysaccharides (LPS) as signaling molecules that affect adipocyte functionality. We tested the effect of increasing concentrations of -derived LPS (10, 100, or 1000 ng/mL) on the 3T3-L1 adipocyte cell line. Exposure to LPS was found to increase the expression of several adipokines (e.g., MIP-2, MCP-1, TNF-, IL-6, lipocalin-2, and FABP4) in 3T3-L1 adipocytes and significantly reduced the expression of leptin and adiponectin. The effects of -derived LPS on MIP-2 expression were similar in comparison with that of LPS prepared from and in our cell culture-based system. This study suggests that -derived LPS functions as a signaling molecule that impacts the inflammatory function of white adipose tissue on the level of gene expression.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5516741PMC
http://dx.doi.org/10.1155/2017/9039302DOI Listing

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